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Poult Sci 2006. 85:2141-2148
© 2006 Poultry Science Association
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IMMUNOLOGY, HEALTH, AND DISEASE

Role of Thyroid Hormones, Maternal Antibodies, and Antibody Response in the Susceptibility to Colibacillosis of Broiler Genotypes

B. Ask*,{dagger},1, E. Decuypere{ddagger} and E. H. van der Waaij{dagger}

* Department of Farm Animal Health, Utrecht University, 3508 TD, The Netherlands; {dagger} Animal Breeding and Genetics Group, Wageningen University, 6700 AH, The Netherlands; and {ddagger} Laboratory for Physiology of Domestic Animals, Department of Animal Production, Katholieke Universiteit Leuven, 3001, Belgium

1 Corresponding author: birgitte.ask{at}wur.nl


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
The purpose of this study was to investigate whether differences in susceptibility to colibacillosis are associated with maternal antibodies, antibody response, and alterations in thyroid hormones [triiodothyronine (T3) and thyroxine (T4)] and to investigate the effect of genotype on the changes in T3 and T4 during challenge and antibody response. A challenge experiment was executed in 2 trials. Per trial, 24 chicks per genotype were challenged, and 20 chicks per genotype were controls. At 7 d of age, challenged chicks were intratracheally inoculated with 0.3 mL of Escherichia coli O78K80 and controls with 0.3 mL of PBS. All chicks were euthanized at 14 or 15 d. Thyroid hormone plasma concentrations and E. coli-specific antibody titers (AB) were measured at 7 d (T3 d7, T4 d7, and ABd7) and 14 or 15 d (change from 7 to 14 or 15 d was analyzed: {Delta}T3, {Delta}T4, and {Delta}AB). Susceptibility was defined based on mortality, lesions, growth retardation, and eating behavior. There was a significant effect of challenge on T3 d7; probably due to eating pattern in association with circadian rhythm. The challenge group was suggested to have functional hypothyroidism relative to the control group, indicating metabolic changes due to the challenge, and it was indicated that an antibody response was elicited. Differences in susceptibility were not significantly related to differences in T3 d7, T4 d7, {Delta}T3, or {Delta}T4 or to maternal antibodies (ABd7), but the antibody response tended to increase (decreasing {Delta}AB) with increasing susceptibility. There were indications of genetic variation in T4 d7, {Delta}T4, ABd7, and {Delta}AB, but there was no observed effect of genotype on {Delta}T3 and {Delta}T4 during challenge or on the antibody response. Further, there were indications that selection for growth traits has resulted in alterations in {Delta}T4 due to challenge, as indicated by a lower {Delta}T4 in the challenge group relative to the control group for more intensively selected genotypes as opposed to a higher {Delta}T4 for less intensively selected genotypes.

Key Words: triiodothyronine • thyroxine • antibody response • broiler • susceptibility


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Colibacillosis is a frequent occurring respiratory disease in broilers caused by the Escherichia coli bacterium, which has adverse effects on growth and health, growth retardation being the main problem (Goren, 1991; Vandemaele et al., 2002). Recently, it has been established that even in the face of a severe E. coli challenge, there is considerable variation in the susceptibility to colibacillosis, as expressed by gross lesions, growth retardation, and eating behavior (Ask et al., 2006b). Moreover, it has been found that the susceptibility is subject to genetic variation (Ask et al., 2006a), which offers prospects for selection against susceptibility. However, the biological background (e.g., physical, physiological, ethological, and immunological factors) of the variation in susceptibility to colibacillosis is not yet fully understood, although this is essential to foresee potential (negative) side effects of selection. In this study, we attempted to gain insight into metabolic changes and immune response to an E. coli challenge and their relationship with susceptibility to colibacillosis.

In the face of a pathogenic challenge, an animal may be able to cope without showing growth retardation and eliciting an immune response if it possesses sufficient maternal or innate immunity (in the form of physical, chemical, or biological barriers) to resist the challenge. If this is not the case, however, the animal must elicit an immune response. Eliciting an immune response also involves significant metabolic changes [i.e., a general increase in metabolic energy expenditure and net proteolysis and lipolysis (Beisel, 1975)] and a reduction in appetite (Sonti et al., 1996), which, on their own or combined, result in growth retardation (Klasing and Johnstone, 1991). Improved knowledge on metabolic changes, maternal immunity, as well as on immune response could therefore provide insight into the biological background of the observed variation in susceptibility to colibacillosis.

The thyroid hormones [triiodothyronine (T3) and thyroxine (T4)] are key elements in metabolism, affecting general metabolic rate as well as protein and adipose turnover rates (Reece, 1997), and information on the levels and changes in these hormones during challenge may therefore be a relatively informative indicator of metabolic changes during challenge. Antibody response is part of the humoral immune response but may also function as a relatively informative indicator of an immune response in general, because the humoral immune response depends on an activation of the innate immune response (Tizard, 2004).

Alternatively to coping with a pathogenic challenge through sufficient maternal or innate immunity, an altered regulation of metabolism and appetite during an infection in broilers may also allow a broiler to cope without showing growth retardation. The metabolic changes that are normally involved in an immune response (innate or humoral) make sense from an evolutionary and a teleological point of view: For an effective immune response, the requirements for resources are usually acute, but, in the wild, obtaining feed and converting feed into energy and protein is costly and time-consuming, and the possibility to acquire external resources is decreased in an infected animal. In contrast, in an environment with ad libitum and easy accessible feed, the use of body reserves as a source of energy and protein and the cessation of eating during infection may not be the most sensible strategy. The intensive selection for growth in broilers in an environment with ad libitum and easy accessible feed may contribute to a change in coping strategy through changes in prioritization of body functions toward growth rather than "traditional" fitness traits, such as disease resistance. It is therefore hypothesized that the regulation of metabolic changes and appetite in broilers during an immune response (innate or humoral) is altered, and differences among broiler genotypes may provide insight into this matter.

The purpose of this study was 2-fold: 1) to investigate whether differences in susceptibility to colibacillosis are associated with maternal antibodies, antibody response, and alterations in T3 and T4 hormones; and 2) to investigate the effect of genotype on the changes in T3 and T4 during challenge and on antibody response.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
A challenge experiment was carried out on a population consisting of multiple broiler lines and crosses to ensure a broad genetic inference of results. The susceptibility of the individual lines and crosses to colibacillosis is presented in Ask et al. (2006a).

Chicks
Eggs were incubated (at 37.8°C) and hatched (34°C in hatcher) in 2 trials at the Spelderholt Institute for Poultry Research in Beekbergen, The Netherlands. The eggs originated from 6 pure broiler lines: 2 sire [Sire1 (A2) and Sire2 (E3)], 3 dam [Dam1 (A3), Dam2 (E4), and Dam3 (E5)], and 1 slow-growing line [SlowGrow (3)] and 2 crosses: a sire and a dam cross [SireCross (A2 x E3) and DamCross (A3 x E4)]. Henceforward, the lines and crosses together will be referred to as genotypes. At the time of egg collection, the age of the parent stock of the slow-growing line was 47 wk (trial 1) or 50 wk (trial 2), whereas the age of the parent stocks for the other genotypes was 27 wk (trial 1) or 30 wk (trial 2). All parent stock, except for that of the SlowGrow, was kept in groups at the pure-line pedigree farm in Herveld, The Netherlands, which is foreseen with a filtered air and positive pressure system. The SlowGrow parent stock was kept at a separate commercial production unit. A total of 240 eggs were incubated from each of the Dam1, Dam2, Dam3, Dam-Cross, and SlowGrow genotypes. From each of the Sire1 and Sire2 genotypes, a total of 300 eggs were incubated, and from the SireCross, a total of 293 eggs were incubated. The hatchabilities of the respective genotypes were 82% (Dam1), 76% (Dam2), 81% (Dam3), 66% (DamCross), 88% (SlowGrow), 40% (Sire1), 52% (Sire2), and 58% (SireCross).

Experimental Design
At 1 d of age (at hatch), the chicks were individually tagged with badges and allocated randomly to a challenge and a control group, each with 4 pens. In each trial, there were 192 chicks in the challenge group (48 chicks per pen) and 160 chicks in the control group (40 chicks per pen). There were more chicks in the challenge group than in the control group to anticipate losses due to mortality. Genotype and sex were equally represented: In each pen in the challenge group, there were 3 males and 3 females per genotype. In the control group, there were 3 males and 2 females per genotype in each of 2 of the 4 pens and 2 males and 3 females per genotype in the other 2 pens.

The challenge and the control group were kept in separate but identical climate-controlled cells to avoid horizontal infection of control chicks. The pens in both groups each covered an area of 1.54 x 1.75 m, had walls that were 0.5 m high, and were provided with litter in the form of sawdust. Feed and water were provided ad libitum. The feed was a commercial standard mix for starters with 12.77 MJ of ME and 20.8% CP. A schedule of 20L:4D was practiced with lights on at 0600 h. The temperature followed a standard schedule, starting at 34°C at 1 d of age, followed by a gradual decline to 24°C at 15 d of age. The humidity was kept at 50%.

Challenge
At 7 d of age, all chicks in the challenge group were individually inoculated intratracheally with a 1:100 PBS of an E. coli O78K80 (506) strain cultured in glucose peptone broth. The inoculation was done using a 1.0-mL syringe fitted with a blunt-ended pipette tip (4862, Corning Inc., Corning, NY). The E. coli 506 strain was a flumequine-resistant strain isolated from an inflamed pericardium of a commercial broiler suffering from natural colibacillosis (van Eck and Goren, 1991). In the first trial, 25 chicks from 1 pen were inoculated with 0.5 mL of E. coli solution with a total of 106.3 cfu, but 4 of these chicks showed signs of suffocation within 15 min postinoculation. For the remainder of the chicks, the volume was therefore adjusted to 0.3 mL, with a total of 106.0 cfu in trial 1 and 105.8 cfu in trial 2. All chicks in the control group were inoculated intratracheally with 0.3 mL of PBS.

Chicks that died during the experiment were dissected, and a macroscopic examination was done. Lesions were not scored. A bacteriological examination of the spleen of all chicks that died during the experiment was performed, and the sensitivity of the E. coli isolates was compared with that of the E. coli 506 strain, as described by Velkers et al. (2005). The cause of death was considered to be colibacillosis if there were signs of airsacculitis, pericarditis, or perihepatitis or if the E. coli strain 506 could be isolated from the spleen. According to this definition, there was 1 chick that did not die due to colibacillosis.

The chick that did not die due to colibacillosis, was omitted from the analyses, as were the 25 chicks that received 0.5 mL of E. coli inoculate and the 9 chicks that died before the inoculation (6 in the challenge group and 3 in the control group).

Recording of Traits
Mortality was recorded every morning. The surviving chicks were stunned by electrocution and euthanized by bleeding; half of the challenge and the control group were euthanized at 14 d of age and the other half at 15 d of age. The following lesion types were scored macroscopically: airsacculitis (right and left thoracic air sac), pericarditis, and perihepatitis. Airsacculitis was considered as representative for E. coli pathology of the respiratory tract, whereas pericarditis and perihepatitis were considered as representative for systemic E. coli pathology. Lesion scoring was performed as described by van Eck and Goren (1991).

Chicks were individually weighed at 1, 4, 7, 10, and 12 d of age, and half of the challenge and control pens were weighed at 14 d of age and the other half at 15 d of age. The BW at 14 or 15 d of age was treated as 1 trait.

At 7 d of age, starting at 0700 h until ~1500 h, blood samples (~1 mL) of individual chicks were taken from the wing vein with a 2.0 syringe and 0.5 x 16 mm needle and subsequently transferred to a heparine- (thromboliquine) coated, round-bottomed polystyrene tube. The syringe and needle were coated with heparine immediately before the sampling. At 14 and 15 d of age, 2 blood samples per individual were collected from the jugular vein (euthanization by bleeding) directly into round-bottomed polystyrene tubes either coated with heparine or un-coated.

Levels of T3 and T4 were measured in the plasma by RIA, as described by Darras et al. (1992), and expressed in nanograms per milliliter. Intraassay CV were 2.5 and 7.5% for T3 and T4, respectively. Antisera as well as T3 and T4 standards were obtained from Byk-Belga NV (Brussel, Belgium).

Antibody titers (IgG; AB) specific to the E. coli O78K80 (506) were determined in the plasma by ELISA, as described by Leitner et al. (1990). The detection antibody used was R{alpha}Ch IgG(H+L)/PO. An E. coli solution of 5 x 108 concentration was heated in warm water (60°C) for 1 h and subsequently sonicated for 1 min. The extinction was measured at 450 nm and expressed as the AB = [critical value – logit(Exti)]/slope, where the critical value is the value on the standard curve at the critical cutoff point; logit(Exti) = ln[Exti/(Emax – Exti)], and slope is the linear slope of the standard curve.

Data Analysis
An ANOVA was used to test for the effect of treatment [i.e., control or challenge group (Model A) and susceptibility to colibacillosis (Model B) on T3 and T4 plasma levels at 7 d of age (T3 d7 and T4 d7, respectively), the change in T3 and T4 plasma levels from 7 to 14 d of age ({Delta}T3 and {Delta}T4, respectively), the E. coli specific IgG AB at 7 d of age (ABd7), and the change in this titer from 7 to 14 d of age ({Delta}AB). An ANOVA was also used to test for an interaction between genotype and treatment (Model C) on {Delta}T3, {Delta}T4, and {Delta}AB. Based on the mortality, lesions, growth retardation, and feeding inhibition, the susceptibility to colibacillosis was defined as 4 categories with increasing susceptibility: 1) chicks without lesions, 2) chicks with airsacculitis and no systemic lesions, 3) chicks with systemic lesions, and 4) chicks that died. The chicks with systemic lesions and chicks that died showed growth retardation, whereas the other chicks did not (Ask et al., 2006b). The t-test was applied to test the effect of each level of susceptibility to colibacillosis and the effect of challenge within genotypes, using Tukey’s adjustment (the Tukey-Kramer method) to correct for multiple comparisons. The models were


Formula 1([A])

where Yijklm = the individual T3 d7, T4 d7, {Delta}T3, {Delta}T4, ABd7, or {Delta}AB in the ith trial (TRIALi); the jth treatment: control or challenge group (CONTCHALj); the kth sex (SEXk); the lth genotype (GENOTYPEl); and the mth age at which measurements at 14 or 15 d of age were done (DAY1415m); µijklm = the mean; and eijklm = the random residual effect.


Formula 2([B])

where Yijklm = the individual T3 d7, T4 d7, {Delta}T3, {Delta}T4, ABd7, or {Delta}AB in the ith trial (TRIALi); the jth category of susceptibility (SUSCEPTj); the kth sex (SEXk); the lth genotype (GENOTYPEl); and the mth age at which measurements at 14 or 15 d of age were done (DAY1415m); µijklm = the mean; and eijklm = the random residual effect.


Formula 3([C])

where Yijklmn = the individual {Delta}T3, {Delta}T4, or {Delta}AB in the ith trial (TRIALi); the jth treatment: control or challenge group (CONTCHALj); the kth sex (SEXk), the lth genotype (GENOTYPEl); the mth interaction between genotype and CONTCHAL (GENOTYPE x CONTCHALm); and the nth age at which measurements at 14 or 15 d of age were done (DAY1415n); µijklmm = the mean; and eijklmn = the random residual effect.

Pearson’s correlations, within control and challenge group, were calculated between individual BW at 7, 10, 12, and 14 d of age and {Delta}T3 or {Delta}T4. In addition, correlations within control and challenge group were calculated between individual {Delta}AB and {Delta}T3 or {Delta}T4. The correlations were based on data corrected for trial, sex, genotype, and the age at which measurements at 14 or 15 d of age were done.

Ethics
The experiment was approved by the Animal Ethics Committee (Dierexperimentencommissie, Utrecht University, The Netherlands), and chicks were handled accordingly. The Animal Ethics Committee based its decision on "De Wet op Dierproeven" (1996) and on the "Dierproevenbesluit" (1985; http://www.nca-nl.org/).


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
In Table 1Go, T3 d7 and {Delta}T3 in the control and challenge group is given. The T3 d7 was 57% higher in the challenge group than in the control group (P < 0.001), but the increase in T3 from 7 to 14 d of age was 45% lower (P = 0.032) in the challenge group than in the control group. There was no significant effect of susceptibility on neither T3 d7 (P ≥ 0.584 for all pairwise comparisons) nor {Delta}T3 (P ≥ 0.671 for all pairwise comparisons), although {Delta}T3 was 42% higher in the chicks with airsacculitis than in the chicks without lesions and 97% higher than that of the chicks with systemic lesions.


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  		Table 1. The plasma levels of T3 and T4 ± SE at 7 d of age (T3 d7 and T4 d7, respectively) in ng/mL and the absolute change SE from 7 to 14 d of age ({Delta}1±T3 and {Delta}T4, respectively) in the control and challenge group and in the challenge group, depending on susceptibility to colibacillosis. The data were analyzed with an ANOVA, adjusting for trial, sex, genotype, and age at measurement2
 
The T4 d7 and {Delta}T4 in the control and challenge group is also given in Table 1Go. There was no significant difference between control and challenge group for T4 d7 (P = 0.283) or for {Delta}T4 (P = 0.660). There was also no significant effect of susceptibility on T4 d7 (P ≥ 0.927 for all pairwise comparisons) or on {Delta}T4 (P ≥ 0.704 for all pairwise comparisons), although {Delta}T4 was 32% higher in the chicks with systemic lesions than in the chicks without lesions and the chicks with airsacculitis.

In Table 2Go, the T3 d7, {Delta}T3, T4 d7, and {Delta}T4 in the control and challenge group are given for the 8 genotypes. There was a significant effect of genotype on T4 d7 (P < 0.001) and {Delta}T4 (P = 0.004), but not on T3 d7 (P = 0.126) or {Delta}T3 (P = 0.321). There was no significant interaction between genotype and challenge for neither {Delta}T3 (P = 0.690) nor {Delta}T4 (P = 0.417). Within genotypes, the only significant difference between control and challenge group was in the Sire2 for {Delta}T3 (P = 0.050) and in the Sire1 for {Delta}T4 (P = 0.029).


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  		Table 2. The plasma levels of T3 and T4 ± SE at 7 d of age (T3 d7 and T4 d7, respectively) in ng/mL and the absolute change ± SE from 7 to 14 d of age ({Delta}T3 and {Delta}T4, respectively) in the control and challenge group1 for the 8 genotypes 2
 
In Table 3Go, the ABd7 and {Delta}AB in the control and challenge group are given. There was no significant effect of neither challenge (P = 0.276) nor susceptibility (P ≥ 0.770 for all pairwise comparisons) on ABd7, whereas {Delta}AB was 41% lower (absolute) in the challenge than in the control group (P = 0.004). There was no significant effect of susceptibility (P ≥ 0.955 for all pairwise comparisons) on {Delta}AB, although {Delta}AB in the chicks without lesions was 24% higher (absolute) than in the chicks with airsacculitis only and 26% higher (absolute) than in the chicks with systemic lesions.


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  		Table 3. The Escherichia coli-specific IgG antibody titer ± SE at 7 d of age (ABd7) and the absolute change ± SE from 7 to 14 d of age ({Delta}AB) in the control and challenge group1 and in the challenge group depending on susceptibility to colibacillosis2
 
In Table 4Go, the ABd7 and {Delta}AB in the control and challenge group are given for the 8 genotypes. There was a significant effect of genotype on both ABd7 (P < 0.001) and {Delta}AB (P < 0.001), but there was no significant interaction between treatment and genotype on {Delta}AB (P = 0.107). Within genotypes, the only significant difference between control and challenge group in {Delta}AB was in the DamCross (P = 0.024) and the SireCross (P = 0.004).


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  		Table 4. The Escherichia coli-specific IgG antibody titer ± SE at 7 d of age (ABd7) and the absolute change ± SE from 7 to 14 d of age ({Delta}AB) in the control and challenge group1 for the 8 genotypes2
 
The correlations within control and challenge group between BW at 7, 10, 12, and 14 d of age and {Delta}T3 or {Delta}T4 were all small and nonsignificant (ranging from 0.08 ± 0.25 to 0.10 ± 0.15). The correlations within control and challenge group between {Delta}AB and {Delta}T3 or {Delta}T4 were all small and nonsignificant as well (ranging from –0.02 ± 0.82 to –0.08 ± 0.23).


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
To compare temporal change in plasma T3 and T4 and E. coli-specific IgG antibody levels in the challenge group relative to the control group, it is of importance that the groups are similar before the challenge with regards to these parameters. In this study, this was the case for both T4 d7 and ABd7, as the control and challenge groups did not differ significantly (Tables 1Go and 3Go). The nonsignificant difference in ABd7 between the control and challenge group suggests that there were no differences between the groups in maternal antibodies. In contrast, T3 d7 was found to be 57% higher in the challenge than in the control group (Table 1Go). This difference is probably related to the differential timing of the blood sampling, as samples were taken from the challenge group from 1 to 5 h after lights on and from 5 to 9 h after lights on from the control group. The eating pattern of broilers is known to be affected by the circadian rhythm; for example, a relatively large peak in feed intake is generally observed within 2 to 3 h after lights on. This peak is associated with an increased T3 plasma level (Decuypere and Kühn, 1984). Therefore, eating pattern in association with circadian rhythm may explain the observed difference in T3 d7.

The {Delta}T3 was found to be lower in the challenge group than in the control group, whereas {Delta}T4 did not differ significantly between the control and challenge groups (Table 1Go), which suggests functional hypothyroidism in the challenge group relative to the control group. The lower {Delta}T3 in the challenge group indicates that metabolic changes have taken place due to the challenge. The groups of differing susceptibility to colibacillosis did not differ significantly for T3 d7 or T4 d7 (Table 1Go). This suggests that differences in plasma thyroid hormones before challenge did not influence the susceptibility to the challenge.

Based on this experiment, susceptibility to colibacillosis, as indicated by gross lesions and mortality, was found to be associated with growth retardation (Ask et al., 2006b) and reduced eating behavior, indicating reduced feed intake (Ask et al., 2004). Previously, a positive association has been observed between growth and T3 in the plasma, and a negative association has been observed between growth and T4 in the plasma (Lauterio et al., 1986; Decuypere and Buyse, 1988). Reversely, many studies have shown that feed restriction leads to reduced T3 plasma levels and increased T4 plasma levels (May, 1978; Darras et al., 1995; Van der Geyten et al., 1999). These associations between growth or feed intake and thyroid hormones could, however, not be confirmed by this study, because the groups of differing susceptibility to colibacillosis did not differ significantly for neither {Delta}T3 nor {Delta}T4 (Table 1Go). It should be noted, however, that the group with systemic lesions (and growth retardation and absence of eating behavior) did have both the lowest {Delta}T3 and the highest {Delta}T4 of all the groups.

The {Delta}AB was found to be lower (in absolute terms) in the challenge group than in the control group (Table 3Go), thereby indicating an elicitation of an antibody response. This can be explained as follows: In the control group, a negative {Delta}AB was expected due to the degradation of maternal antibodies. In the challenge group, if no antibody response was elicited, the {Delta}AB was expected to be either more negative than in the control group (in case of a systemic infection), because of the formation of antibody-antigen complexes or not to differ from the control group (in case of a nonsystemic infection). This study is therefore in agreement with the theory that an immune response (innate or humoral) is accompanied by metabolic changes, as previously observed in, for example, an increased fractional disappearance rate of T3 in the plasma (Beisel, 1975). There was no significant difference in ABd7 among groups of differing susceptibility to colibacillosis, either (Table 3Go). This suggests that the differences in susceptibility to colibacillosis were not related to differences in maternal antibodies. The E. coli specific antibody response tended to increase (decreasing {Delta}AB) with increasing susceptibility (Table 3Go).

The low and nonsignificant correlations between {Delta}AB and {Delta}T3 or {Delta}T4 suggested that there was no association between the thyroid hormone changes in the plasma during the challenge and the elicitation of a specific antibody response to the challenge.

There was a significant effect of genotype on T4 d7, {Delta}T4, ABd7, and {Delta}AB, thereby indicating the presence of genetic variation in these traits, which is in agreement with previous studies (Bowen and Washburn, 1984; Cheng et al., 1991; Yonash et al., 1996). The effect of genotype on T3 d7 and {Delta}T3 was not significant. Although this is not indicative of the presence of genetic variation, it is also not indicative of the absence of genetic variation and therefore not in disagreement with the previous finding of genetic variation in the T3 plasma level (Bowen and Washburn, 1984). The absence of a significant interaction between genotype and challenge in all traits suggested that genotype does not have an effect on the changes in T3 and T4 plasma levels during challenge and also not on the specific antibody response to challenge. Previously, several studies have suggested that the regulation of T3 and T4 has been altered in commercial broilers due to the intensive selection for growth traits, although there is controversy on whether this is expressed in the form of functional hypothyroidism (relatively low T3 but unchanged T4 levels; May and Marks, 1983; Gonzales et al., 1999) or functional hyperthyroidism (relatively high T3 but unchanged T4 levels; Decuypere and Kühn, 1988). Because the SlowGrow was less intensively selected than the other genotypes in this study, it was therefore also expected that the other genotypes would express some degree of functional hypothyroidism or hyperthyroidism relative to the SlowGrow. Neither of the 2 could be confirmed though, as differences between the SlowGrow and the other genotypes were nonsignificant for both {Delta}T3 and {Delta}T4 (Table 2Go). There were indications of alterations in the T4 plasma level during challenge due to selection for growth traits, however. The genotypes that have been selected relatively less intensively for growth traits (the SlowGrow and the 3 dam genotypes) tended to respond differently to the E. coli challenge with regards to {Delta}T4 than the genotypes that have been selected relatively more intensively for growth traits (the 2 sire genotypes and the SireCross). In the genotypes selected relatively less intensively for growth traits, the {Delta}T4 was higher in the challenge than in the control group, whereas the opposite was found in the genotypes selected more intensively for growth traits (Table 2Go).

The {Delta}AB within genotypes only differed significantly between control and challenge group for the DamCross and the SireCross, but, in general, there was a tendency to a lower (in absolute terms) {Delta}AB in the challenge than in the control group (except for the Dam3 and Sire1; Table 4Go). As mentioned above, this is indicative of an elicitation of an antibody response. Previously, it has been shown that less intensively selected broilers (broilers randomly selected since 1957) have a higher humoral immune response than more intensively selected broilers (commercial broiler strains from 1991 and 2001; Qureshi and Havenstein, 1994; Cheema et al., 2003), but in this study, the differences in {Delta}AB between the genotypes that have been selected relatively more or less intensively for growth traits could not support such an effect of selection.

In general, it should further be noted that even though most pairwise comparisons among genotypes were statistically nonsignificant, several were large (e.g., in the challenge group, {Delta}T3 was more than 11 times as large in Sire2 as in Sire1), and it cannot be ruled out that such large differences may be of biological significance.

To summarize, there were both an E. coli-specific antibody response and thyroid hormone changes in the plasma in response to challenge. There were, however, only indications of an association between susceptibility to colibacillosis and the thyroid hormone changes or the E. coli-specific antibody response, and there was no association between maternal antibodies and susceptibility to colibacillosis. The biological background of the differences in susceptibility to colibacillosis is therefore still unclear, but part of the explanation may be found in other metabolism or immune response-related parameters than the ones measured here. There was genetic variation present in both the T4 plasma level and the E. coli-specific antibody response, but genotype did not have a significant effect on {Delta}T3 or {Delta}T4 during challenge and also not on the specific antibody response to challenge. Further, there were indications of alterations in {Delta}T4 during challenge due to the selection for growth traits, as indicated by a lower {Delta}T4 in the challenge group relative to the control group for more intensively selected genotypes as opposed to a higher {Delta}T4 for less intensively selected genotypes.


   ACKNOWLEDGMENTS
 
We thank Ger van der Vries Reilingh and Gerda Nackaerts for their helpful, professional, and friendly technical assistance regarding the measurements of the AB and thyroid hormone levels. We also thank the Adaptation and Physiology Group, Wageningen University, for making their laboratory at our disposal. Further, we thank Hybro BV, Boxmeer, The Netherlands for providing the broiler genotypes, and, last but not least, we thank Sander van Voorst and Jan Hoekman from Spelderholt for their professional assistance with the execution of the experiment.

Received for publication March 30, 2006. Accepted for publication July 18, 2006.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
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