Background: Swine farmers repeatedly exposed to the barn air suffer from respiratory diseases. However the mechanisms of lung dysfunction following repeated exposures to the barn air are still largely unknown. Therefore, we tested a hypothesis in a rat model that multiple interrupted exposures to the barn air will cause chronic lung inflammation and decline in lung function.

The authors tested a hypothesis that lung inflammation and airway hyperresponsiveness (AHR) induced following barn air exposure are dependent on Toll-like receptor 4 (TLR4) by exposing C3HeB/FeJ (intact TLR4, wild type [WT]) and C3H/HeJ (defective TLR4, mutant) mice either to the barn air (8 hours/day for 1, 5, or 20 days) or ambient air. Both strains of mice, compared to their respective controls, showed increased AHR following 5 exposures but dampened AHR after 20 exposures to show lack of effect of TLR4 on AHR. However, swine barn air induced lung inflammation with recruitment of inflammatory cells and cytokine expression was observed in WT but not in mutant mice. These data show different roles of TLR4 in lung inflammation and AHR in mice exposed to swine barn air.

A lack of appropriate disease models has limited our understanding of the pathogenesis of persistent enteric infections with Mycobacterium avium subsp. paratuberculosis. A model was developed for the controlled delivery of a defined dose of M. avium subsp. paratuberculosis to surgically isolated ileal segments in newborn calves. The stable intestinal segments enabled the characterization of host responses to persistent M. avium subsp. paratuberculosis infections after a 9-month period, including an analysis of local mucosal immune responses relative to an adjacent uninfected intestinal compartment. M. avium subsp. paratuberculosis remained localized at the initial site of intestinal infection and was not detected by PCR in the mesenteric lymph node. M. avium subsp. paratuberculosis-specific T cell proliferative responses included both CD4 and ␥␦ T cell receptor (␥␦TcR) T cell responses in the draining mesenteric lymph node. The levels of CD8 ؉ and ␥␦TcR ؉ T cells increased significantly (P < 0.05) in the lamina propria, and M. avium subsp. paratuberculosis-specific tumor necrosis factor alpha (TNF-␣) and gamma interferon secretion by lamina propria leukocytes was also significantly (P < 0.05) increased. There was a significant (P < 0.05) accumulation of macrophages and dendritic cells (DCs) in the lamina propria, but the expression of mucosal toll-like receptors 1 through 10 was not significantly changed by M. avium subsp. paratuberculosis infection. In conclusion, surgically isolated ileal segments provided a model system for the establishment of a persistent and localized enteric M. avium subsp. paratuberculosis infection in cattle and facilitated the analysis of M. avium subsp. paratuberculosis-specific changes in mucosal leukocyte phenotype and function. The accumulation of DC subpopulations in the lamina propria suggests that further investigation of mucosal DCs may provide insight into host responses to M. avium subsp. paratuberculosis infection and improve vaccine strategies to prevent M. avium subsp. paratuberculosis infection.

Agriculture environments contain a variety of inflammatory aerosols that may increase risk for lung inflammation and disease in exposed individuals. In addition, epidemiological studies have also identified protective effects of rural environments and farming exposures. In this review, we will discuss recent literature published since 2016 that investigates the impact of differing agricultural exposures on respiratory health. Discussions include the impact of farming modernization, education and personal protective equipment usage amongst workers, timing and duration in mediating lung health outcomes, and population studies investigating the association between exposure and risk for numerous lung diseases.

Sepsis induces recruitment of neutrophils and monocytes/macrophages in the lung and enhances host susceptibility to a secondary bacterial challenge. The phenotype and functions of recruited pulmonary intravascular monocytes/macrophages (PIMMs) in sepsis remain largely unknown. Therefore, we characterized PIMM recruitment and functions in a rat model of E. coli-induced sepsis. Male Sprague-Dawley rats were injected intraperitoneally with saline (n ¼ 10) and 48 hr after the saline treatment treated intravenously with either saline (n ¼ 5) or E. coli lipopolysachharide (LPS; 1.5 mg/kg body weight; n ¼ 5). A second group of 10 rats was infected intraperitoneally with E. coli (2 3 10 7 CFU/100 g) followed by intravenous injection of either saline (n ¼ 5) or LPS (n ¼ 5) 48 hr after the first treatment. Rats were euthanized at 6 hr after LPS treatment. Immunocytochemistry showed more PIMMs stained with ED-1 antibody, which specifically reacts with rat monocytes/macrophages, in rats infected with E. coli compared with the controls (P < 0.05). LPS treatment of E. coli-infected rats increased the numbers of PIMMs (P < 0.05) and induced more inflammation compared to other groups. Immuno-electron microscopy localized TNF-a, IL-10, and TGF-b2 in recruited PIMMs in rats challenged with both E. coli and LPS. ELISA on lung homogenates showed higher concentrations of TNF-a, IL-10, and TGF-b2 in rats treated with both E. coli and LPS compared with those treated with only LPS or E. coli (P < 0.05). We conclude that ED-1-positive PIMMs are recruited in this model of sepsis and contain TNF-a, IL-10, and TGF-b2. Anat Rec Part