A retrospective characterization of pediatric facemasks marketed in the United States and implications for future designs.

Background: Device manufacturers who seek to market their pediatric facemasks in the United States (U.S.), as part of anthropometric data requirement, need to demonstrate their mask designs are expected to fit the intended user population.

Staphylococcal enterotoxins in the etiopathogenesis of mucosal autoimmunity within the gastrointestinal tract.

The staphylococcal enterotoxins (SEs) are the products of Staphylococcus aureus and are recognized as the causative agents of classical food poisoning in humans following the consumption of contaminated food. While illness evoked by ingestion of the SE or its producer organism in tainted food are often self-limited, our current understanding regarding the evolution of S. aureus provokes the utmost concern.

TGF-beta can leave you breathless.

Transforming growth factor-beta (TGF-beta), a ubiquitous and multifunctional cytokine, is central to the evolution and modulation of host defense. Early on, TGF-beta was recognized for its chemotactic and pro-inflammatory properties, but then identification of its powerful suppressive activities focused attention on dissecting its mechanisms of immune inhibition. Just as quickly as TGF-beta-mediated regulation of a population of CD4(+)CD25(+)Foxp3(+) regulatory T cells became the rage, a surprising finding that TGF-beta was the impetus behind a subset of pro-inflammatory T helper (Th)17 cells brought back a re-emphasis on its broader ability to dictate inflammatory events.

Aberrant innate immune responses in TLR-ligand activated HLA-B27 transgenic rat cells.

Background: Commensal enteric microbiota initiate and perpetuate immune-mediated colitis in HLA-B27 transgenic (TG) rats but not wildtype (non-TG) littermates. However, the role of the innate immune response to bacterial components has not been established.

Methods: We examined responses induced by bacterial adjuvants through Toll-like receptor (TLR) and NOD2 signaling in T-cell-depleted splenocytes from HLA-B27 TG rats versus non-TG controls.

Reduced responsiveness of HLA-B27 transgenic rat cells to TGF-beta and IL-10-mediated regulation of IFN-gamma production.

Background: We have reported that commensal luminal bacterial components induce an active in vitro IFN-gamma response in mesenteric lymph node (MLN) and intestinal cells from specific pathogen-free (SPF) HLA-B27 transgenic (TG) rats with chronic colitis but not in cells from non-diseased SPF non-TG, germ-free (GF) non-TG or GF TG rats.

Methods: The study examined IL-12 stimulation of MLN IFN-gamma responses to luminal bacteria and regulation of these responses by suppressive cytokines.

Results: Exogenous IL-12 significantly increased the bacterial lysate-induced IFN-gamma response in SPF TG MLN cells, while bacterial lysate and IL-12 synergistically induced IFN-gamma from low baseline levels in cells obtained from both SPF and GF non-TG rats, and in GF TG cells.

CD4(+) T lymphocytes mediate colitis in HLA-B27 transgenic rats monoassociated with nonpathogenic Bacteroides vulgatus.

Background: HLA-B27/beta2 microglobulin transgenic (TG) rats develop spontaneous colitis when raised under specific pathogen-free (SPF) conditions or after mono-association with Bacteroides vulgatus (B. vulgatus), whereas germ-free TG rats fail to develop intestinal inflammation. SPF HLA-B27 TG rnu/rnu rats, which are congenitally athymic, remain disease free.

Luminal bacterial antigen-specific CD4+ T-cell responses in HLA-B27 transgenic rats with chronic colitis are mediated by both major histocompatibility class II and HLA-B27 molecules.

Rats transgenic (TG) for the human major histocompatibility complex (MHC) class I HLA-B27 and beta2-microglobulin genes develop chronic colitis under specific pathogen-free (SPF) but not sterile (germ-free, GF) conditions. We investigated the role of antigen-presenting molecules involved in generating immune responses by CD4+ mesenteric lymph node (MLN) cells from colitic HLA-B27 TG rats to commensal enteric micro-organisms. All TG MLN cells expressed HLA-B27.

Dysregulated luminal bacterial antigen-specific T-cell responses and antigen-presenting cell function in HLA-B27 transgenic rats with chronic colitis.

HLA-B27/beta2 microglobulin transgenic (TG) rats spontaneously develop T-cell-mediated colitis when colonized with normal commensal bacteria, but remain disease-free under germ-free conditions. We investigated regulation of in vitro T-cell responses to enteric bacterial components. Bacterial lysates prepared from the caecal contents of specific pathogen-free (SPF) rats stimulated interferon-gamma (IFN-gamma) production by TG but not non-TG mesenteric lymph node (MLN) cells.

Reduced susceptibility to dextran sulphate sodium-induced colitis in the interleukin-2 heterozygous (IL-2) mouse.

Summary Mice homozygous for an inactivation of the interleukin-2 (IL-2) gene develop a T-cell dependent colitis. Heterozygous (IL-2+/-) mice are clinically healthy but have been shown to express reduced levels of IL-2 in the colon. Splenocytes from the IL-2+/- mice had a poorer proliferative response to polyclonal T-cell activation and these mice have reduced numbers of intestinal regulatory T cells (CD4+ CD25+ cells) when compared to wild type mice.