Characterizing the immune response of chickens to Campylobacter jejuni (Strain A74C)

Abstract

Campylobacter is one of the major foodborne pathogens causing bacterial gastroenteritis worldwide. The immune response of broiler chickens to C. jejuni is under-researched. This study aimed to characterize the immune response of chickens to Campylobacter jejuni colonization. Birds were challenged orally with 0.5 mL of 2.4 x 108 CFU/mL of Campylobacter jejuni or with 0.5 mL of 0.85% saline. Campylobacter jejuni persisted in the ceca of challenged birds with cecal colonization reaching 4.9 log10 CFU/g on 21 dpi. Campylobacter was disseminated to the spleen and liver on 7 dpi and was cleared on 21 dpi from both internal organs. Challenged birds had a significant increase in anti-Campylobacter serum IgY (14&21 dpi) and bile IgA (14 dpi). At 3 dpi, there was a significant suppression in T-lymphocytes derived from the cecal tonsils of birds in the challenge treatment when compared to the control treatment after 72 h of ex vivo stimulation with Con A or C. jejuni. The T-cell suppression on 3 dpi was accompanied by a significant decrease in LITAF, K60, CLAU-2, IL-1β, iNOS, and IL-6 mRNA levels in the ceca and an increase in nitric oxide production from adherent splenocytes of challenged birds. In addition, on 3 dpi, there was a significant increase in CD4+ and CD8+ T lymphocytes in the challenge treatment. On 14 dpi, both pro and anti-inflammatory cytokines were upregulated in the spleen, and a significant increase in CD8+ T lymphocytes in Campylobacter-challenged birds’ ceca was observed. The persistence of C. jejuni in the ceca of challenged birds on 21 dpi was accompanied by an increase in IL-10 and LITAF mRNA levels, an increase in MNC proliferation when stimulated ex-vivo with the diluted C. jejuni, an increase in serum specific IgY antibodies, an increase in both CD4+ and CD8+ cells, and a decrease in CD4+:CD8+ cell ratio. The balanced Th1 and Th2 immune responses against C. jejuni might explain the ceca’s bacterial colonization and the absence of pathology in Campylobacter-challenged birds. Future studies on T lymphocyte subpopulations should elucidate a pivotal role in the persistence of Campylobacter in the ceca.

Avian Macrophage Responses to Virulent and Avirulent Clostridium perfringens

“…A previous study has shown that chicken bone marrow cultures predominantly containing dendritic cells can respond to bacterial stimulation by upregulating the expression of their costimulatory molecules that included MHC-II, CD40, CD80, and CD86 [31]. A recent study that investigated the ex vivo effects of Campylobacter jejuni on the chicken splenic and cecal tonsil cells showed a significant proliferation of mononuclear cells in response to C. jejuni or concanavalin A mitogen, suggesting a pathogen-induced immunostimulation [32]. Additionally, the authors found that splenocyte expression of the iNOS gene and subsequent production of NO was elevated in response to C. jejuni treatment.…”

Live-Attenuated Oral Vaccines to Reduce Campylobacter Colonization in Poultry

“…Although we did not measure immune response in chickens after oral challenge with the ΔahpC mutant in this study, we can speculate that similar or the same immune responses will be induced in chickens as induced by WT C. jejuni because the mutant is a live C. jejuni strain defective with only a single gene, which can colonize the gastrointestinal tract of chickens ( Figure 1 , Figure 2 and Figure 3 ). In chickens, C. jejuni colonization results in a significant increase in anti- Campylobacter serum IgY and bile IgA [ 36 ], and induces pro-inflammatory responses [ 37 , 38 ]. One of the challenges in Campylobacter control using vaccination is the short life span of commercial broilers, which is usually about several weeks depending on the body weight.…”

“…At this point, we cannot explain the mechanism behind the body weight increase by oral administration with the ΔahpC mutant. It has been suggested that the induction of pro-inflammatory responses by C. jejuni colonization may reduce the body weight of chickens by disrupting nutrient absorption [ 36 , 37 , 38 ]. We observed that the body weight of chickens treated with PBS was always higher than that of those challenged with only WT ( Table 1 ), suggesting C. jejuni colonization can affect the body weight of chickens.…”

Campylobacter jejuni: targeting host cells, adhesion, invasion, and survival

“…Besides these factors, it has to be kept in mind that additionally, the immune defense of the host will have a great influence of colonization and virulence, too. It is known that a balanced Th1 and Th2 immune response against C. jejuni might explain the bacterial colonization of the caecum and the absence of pathology in infected chickens (Mortada et al 2021 ).…”