Absence of Nucleotide-Oligomerization-Domain-2 Is Associated with Less Distinct Disease in Infected Secondary Abiotic IL-10 Deficient Mice.

Human -infections are progressively increasing worldwide. Despite their high prevalence and socioeconomic impact the underlying mechanisms of pathogen-host-interactions are only incompletely understood. Given that the innate immune receptor nucleotide-oligomerization-domain-2 (Nod2) is involved in clearance of enteropathogens, we here evaluated its role in murine campylobacteriosis.

Small Intestinal Pro-Inflammatory Immune Responses Following Infection of Secondary Abiotic IL-10 Mice Lacking Nucleotide-Oligomerization-Domain-2.

Host immune responses are crucial for combating enteropathogenic infections including . Within 1 week following peroral infection, secondary abiotic IL-10 mice develop severe immunopathological sequelae affecting the colon (ulcerative enterocolitis). In the present study, we addressed whether pathogen-induced pro-inflammatory immune responses could also be observed in the small intestines dependent on the innate receptor nucleotide-oligomerization-domain-protein 2 (Nod2).

Immune responses upon infection of secondary abiotic mice lacking nucleotide-oligomerization-domain-2.

Background: infections are of rising importance worldwide. Given that innate immune receptors including nucleotide-oligomerization-domain-2 (Nod2) are essentially involved in combating enteropathogenic infections, we here surveyed the impact of Nod2 in murine campylobacteriosis.

Methods And Results: In order to overcome physiological colonization resistance preventing from infection, we generated secondary abiotic Nod2 and wildtype (WT) mice by broad-spectrum antibiotic treatment.

Microbiota Composition and Immune Responses During Infection in Conventionally Colonized IL-10 Mice Lacking Nucleotide Oligomerization Domain 2.

Host immune responses are pivotal for combating enteropathogenic infections. We here assessed the impact of the innate receptor nucleotide oligomerization domain protein 2 (NOD2) in murine -infection. Conventionally colonized IL-10 mice lacking NOD2 and IL-10 controls were perorally challenged with strain 81-176 and displayed comparable pathogenic colonization of intestines until day 14 postinfection (p.

infection of conventionally colonized mice lacking nucleotide-oligomerization-domain-2.

Background: The nucleotide-binding oligomerisaton protein 2 (NOD2) constitutes a pivotal sensor of bacterial muramyl dipeptide and assures expression of distinct antimicrobial peptides and mediators produced by enterocytes and immune cells directed against pathogens including . We here elucidated the role of NOD2 during murine infection in more detail.

Results: Conventionally colonized NOD2 deficient (NOD2) mice and corresponding wildtype (WT) counterparts were perorally infected with strain 81-176 on three consecutive days.

Colonic Expression of Genes Encoding Inflammatory Mediators and Gelatinases During Campylobacter Jejuni Infection of Conventional Infant Mice.

Within 1 week following peroral Campylobacter jejuni infection, infant mice develop acute enteritis resolving thereafter. We here assessed colonic expression profiles of mediators belonging to the IL-23/IL-22/IL-18 axis and of matrix-degrading gelatinases MMP-2 and MMP-9 at day 6 post C. jejuni strain 81-176 infection.

The Role of IL-23, IL-22, and IL-18 in Campylobacter Jejuni Infection of Conventional Infant Mice.

We have recently shown that, within 1 week following peroral Campylobacter jejuni infection, conventional infant mice develop self-limiting enteritis. We here investigated the role of IL-23, IL-22, and IL-18 during C. jejuni strain 81-176 infection of infant mice.

The IL-23/IL-22/IL-18 axis in murine Campylobacter jejuni infection.

Background: Human Campylobacter jejuni infections are worldwide on the rise. Information about the distinct molecular mechanisms underlying campylobacteriosis, however, are scarce. In the present study we investigated whether cytokines including IL-23, IL-22 and IL-18 sharing pivotal functions in host immunity were involved in mediating immunopathological responses upon C.

Interleukin-18 Mediates Immune Responses to Campylobacter jejuni Infection in Gnotobiotic Mice.

Background: Human Campylobacter jejuni infections are progressively rising worldwide. Information about the molecular mechanisms underlying campylobacteriosis, however, are limited. In the present study we investigated whether cytokines such as IL-23, IL-22 and IL-18, which share pivotal functions in host immunity, were involved in mediating intestinal and systemic immunopathological responses upon C.

The Role of Gelatinases in Campylobacter Jejuni Infection of Gnotobiotic Mice.

Matrix metalloproteinases (MMP)-2 and -9 (also referred to gelatinases-A and -B, respectively) are upregulated in the inflamed gut of mice and men. We recently demonstrated that synthetic gelatinase blockage reduced large intestinal pro-inflammatory immune responses and apoptosis following murine Campylobacter (C.) jejuni infection.

Matrix Metalloproteinase-2 Mediates Intestinal Immunopathogenesis in Campylobacter Jejuni-Infected Infant Mice.

Increased levels of the matrix metalloproteinases (MMPs)-2 and -9 (also referred to gelatinase-A and -B, respectively) can be detected in the inflamed gut. We have recently shown that synthetic gelatinase blockage reduces colonic apoptosis and pro-inflammatory immune responses following murine Campylobacter (C.) jejuni infection.

Arcobacter butzleri Induce Colonic, Extra-Intestinal and Systemic Inflammatory Responses in Gnotobiotic IL-10 Deficient Mice in a Strain-Dependent Manner.

Background: The immunopathological impact of human Arcobacter (A.) infections is under current debate. Episodes of gastroenteritis with abdominal pain and acute or prolonged watery diarrhea were reported for A.