Indeed, a variety of pili and adhesion molecules also contribute to em Salmonella /em binding and invasion during normal host condition [57] and are likely to promote binding when intestinal homeostasis is usually perturbed [58]

Indeed, a variety of pili and adhesion molecules also contribute to em Salmonella /em binding and invasion during normal host condition [57] and are likely to promote binding when intestinal homeostasis is usually perturbed [58]. Previous reports have demonstrated the ability of probiotic bacteria to decrease pathogen binding and ameliorate mucosal damage elicited by infection. Caco-2 cells subjected to thermal stress. Results Thermal stress increased the cytotoxic effect of both em S /em . Typhimurium (P = 0.0001) and nonpathogenic em E. coli /em K12 (P = 0.004) to Caco-2 cells, and resulted in greater susceptibility of cell monolayers to em S /em . Typhimurium adhesion (P = 0.001). Thermal stress had no significant impact on inflammatory cytokines released by Caco-2 cells, although exposure to em S /em . Typhimurium resulted in greater than 80% increase in production of IL-6 and IL-8. Blocking em Mouse monoclonal antibody to Hsp27. The protein encoded by this gene is induced by environmental stress and developmentalchanges. The encoded protein is involved in stress resistance and actin organization andtranslocates from the cytoplasm to the nucleus upon stress induction. Defects in this gene are acause of Charcot-Marie-Tooth disease type 2F (CMT2F) and distal hereditary motor neuropathy(dHMN) S /em . Typhimurium with anti-ShdA antibody prior to exposure of em Salmonella /em decreased adhesion (P = 0.01) to non-stressed and thermal-stressed Caco-2 cells. Pre-exposure of Caco-2 cells to em L. rhamnosus /em GG significantly reduced em Salmonella /em -induced cytotoxicity (P = 0.001) and em Salmonella /em adhesion (P = 0.001) to Caco-2 cells during thermal stress, while em L. gasseri /em had no effect. Conclusion Results suggest that thermal stress increases susceptibility of intestinal epithelial Caco-2 cells to em Salmonella /em adhesion, and increases the cytotoxic effect of em Salmonella /em during contamination. Use of em L. rhamnosus /em GG as a probiotic may reduce the severity of contamination during epithelial cell stress. Mechanisms by which thermal stress increases susceptibility to em S /em . Typhimurium colonization and by which em L. rhamnosus /em GG limits the severity of contamination XRP44X remain to be elucidated. Background em Salmonella enterica /em are important facultative intracellular pathogens that cause gastroenteritis in humans [1]. The diverse em Salmonella /em genus contains over 2500 serotypes [2], all of which are potentially pathogenic to humans [3]. Specifically, em Salmonella enterica /em serovar Typhimurium ( em S /em . Typhimurium) is usually implicated in human foodborne illnesses and often enters the human food supply via contamination of poultry, pork, beef and dairy products, and nuts such as peanuts and pistachios. In recent years, antibiotic-resistant strains of em Salmonella /em have emerged, and salmonellosis caused by multi-drug resistant em S /em . Newport and em S /em . Typhimurium DT104 has caused great public health concern [4-6]. Adhesion of em Salmonella /em to the intestinal epithelial surface is a key first step in pathogenesis and is central to its colonization of the intestine [7]. Although em Salmonella /em can colonize a healthy host, the greatest risk for intestinal contamination by enteric pathogens may occur during periods of physiological stress. em In vivo /em animal studies have shown that during periods of stress, susceptibility to em Salmonella /em colonization and contamination increases XRP44X [8-10]. Less is known of how physiological stress may influence the conversation of em Salmonella /em with the human intestinal epithelium, although it is likely to follow a similar trend as other animal models. Proposed mechanisms for increased em Salmonella /em colonization during stress have largely focused on the deleterious effect of stress on host immunity. While impaired immune function certainly contributes to stress-related contamination, little information exists about the influence of stress on susceptibility of epithelial cells to contamination. The intestinal epithelium is usually a crucial, but thin, barrier, which is susceptible to perturbation by stress [11,12]. In particular, epithelial damage elicited by stress may expose or cause apical secretion of extracellular matrix proteins such as fibronectin [13], which serves as receptor for the MisL and ShdA adhesion proteins of em S /em . Typhimurium [14,15]. Recent research has indicated that most physiological and psychological stressors have an impact on gut health and susceptibility to enteric pathogens [16]. For the current study, we used high temperature XRP44X (41C, 1 h) to XRP44X examine the influence of stress on em Salmonella /em colonization of cultured intestinal epithelial cells and the effectiveness of probiotic Lactobacilli for altering the outcome of contamination. Core temperatures ranging from 39C to 42.5C are physiologically relevant and have been reported in humans suffering from mild to severe thermal stress [12]. The deleterious effects of XRP44X thermal stress are first manifested in the gut [12] in humans and animals, and we and others have shown that high temperature stress damages the intestinal epithelium using animal and cell culture models [11,17-19]. Therefore, we chose to use thermal stress as a model physiological stressor that, like other physiological or psychological stressors, can alter normal intestinal homeostasis and may influence the outcome of contamination. Specifically, stress due to high temperature (39C C 42C) can elicit enterocyte membrane damage or death [11,18], alter of normal villus/crypt structure [17,18], impair tight junction integrity [20], and may enhance susceptibility to colonization and contamination by enteric microorganisms. Greater vulnerability to enteric microbes is usually demonstrated by increased LPS concentration in the blood following thermal stress [19,21], and indicates that a compromised gut barrier may lead to opportunistic contamination. However, little information exists around the influence of thermal stress on epithelial susceptibility to pathogen binding and cytotoxicity. Inhibition of pathogen adhesion to the intestinal epithelium may prevent colonization and limit opportunity for systemic contamination [8,22]. Certain probiotic bacteria, including em Lactobacillus /em and em Bifidobacteria /em , may be effective in ameliorating unfavorable intestinal effects of stress [23,24] or preventing adhesion and.