Expression of Toll-Like Receptor 4 and Downstream Effectors in Selected Cecal Cell Subpopulations of Chicks Resistant or Susceptible to Salmonella Carrier State

Abstract

Toll-like receptor 4 (TLR4), which recognizes lipopolysaccharide from Gram-negative bacteria, plays a major role in resistance of mice and humans to Salmonella infection. In chickens, Salmonella may establish a carrier state whereby bacteria are able to persist in the host organism without triggering clinical signs. Based on cellular morphological parameters, we developed a method, without using antibodies, to separate three cecal cell subpopulations: lymphocytes, enterocytes, and a population encompassing multiple cell types. We analyzed the mRNA expression of TLR4, interleukin-1␤ (IL-1␤), IL-8, IL-12, and lipopolysaccharide-induced tumor necrosis factor alpha factor (LITAF) in cecal subpopulations of chicks from inbred lines resistant or susceptible to the carrier state infected with Salmonella enterica serovar Enteritidis. The results showed that resistance to the carrier state in chicks is associated with a larger percentage of lymphocytes and with higher levels of expression of TLR4 and IL-8 at homeostasis in the three cell subpopulations, as well as with a higher level of expression of LITAF in lymphocytes during the carrier state. In contrast to the early phase of infection, the carrier state is characterized by no major cell recruitment differences between infected and noninfected animals and no significant modification in terms of TLR4, IL-1␤, IL-8, IL-12, and LITAF expression in all cell subpopulations measured. However, TLR4 expression increased in the lymphocytes of chicks from the susceptible line, reaching the same level as that in infected chicks from the resistant line. These observations suggest that the carrier state is characterized by a lack of immune activation and highlight the interest of working at the level of the cell population rather than that of the organ.

Performance, histomorphology, and Toll-like receptor, chemokine, and cytokine profile locally and systemically in broiler chickens fed diets supplemented with yeast-derived macromolecules

“…Chen et al (2007) showed that increased TLR2b levels are associated with enhanced gastrointestinal epithelial barrier function against pathogens. Various studies have implicated TLR4 in recognition of glucuronoxylomannan (Shoham et al, 2001) and Saccharomyces cerevisiae and Candida albicans derivates (Tada et al, 2002), and resistance to carrier states of Salmonella in chicks is associated with a higher level of expression of TLR4 (Sadeyen et al, 2006;Chaussé et al, 2011). In the present study, an upregulated TLR21 expression was observed in chickens on BMDand YDM-supplemented diets in the cecal tonsil and bursa of Fabricius, whereas expression in the spleen was downregulated in the YDM treatment.…”

“…Under TLR activation, heterophils can produce inflammatory mediators such as cytokines to help induce further immune responses (Farnell et al, 2003;Kogut et al, 2005). In addition, resistance to pathogens, such as Salmonella spp., has closely been associated with an upregulation of TLR, mainly TLR4, and different chemokines and cytokines (Sadeyen et al, 2006;Chaussé et al, 2011). Aberrant expression of TLR2, TLR4, and TLR21 has been associated with susceptibility to Salmonella enterica serovar Enteritidis infection in chickens (Gou et al, 2012).…”

Control of Salmonella Contamination of Shell Eggs—Preharvest and Postharvest Methods: A Review

“…Another resistance‐related factor called Toll‐like receptor 4 belongs to a family of innate immune system receptors involved in the recognition of lipopolysaccharides (LPS) from Gram‐negative bacteria (Calenge and others ; Chaussé and others ).…”

Salmonella enterica Serovar Typhimurium Skills To Succeed in the Host: Virulence and Regulation

“…These carriers are characterized by a symptom-free condition and can act as reservoirs and hence contribute to the propagation of the disease, which is particularly important in the case of food workers. Unfortunately, there is a scarcity of results concerning the immune response and the efficacy of antimicrobial treatment in these silent infections that could be used to develop suitable prophylactic and therapeutic modalities (34)(35)(36).…”