Effect of low-level CO2 on innate inflammatory protein response to organic dust from swine confinement barns.

BACKGROUND: Organic hog barn dust (HDE) exposure induces lung inflammation and long-term decreases in lung function in agricultural workers. While concentrations of common gasses in confined animal facilities are well characterized, few studies have been done addressing if exposure to elevated barn gasses impacts the lung immune response to organic dusts. Given the well documented effects of hypercapnia at much higher levels we hypothesized that CO2 at 8 h exposure limit levels (5000 ppm) could alter innate immune responses to HDE. METHODS: Using a mouse model, C57BL/6 mice were nasally instilled with defined barn dust extracts and then housed in an exposure box maintained at one of several CO2 levels for six hours. Bronchiolar lavage (BAL) was tested for several cytokines while lung tissue was saved for mRNA purification and immunohistochemistry. RESULTS: Exposure to elevated CO2 significantly increased the expression of pro-inflammatory markers, IL-6 and KC, in BAL fluid as compared to dust exposure alone. Expression of other pro-inflammatory markers, such as ICAM-1 and matrix metalloproteinase-9 (MMP-9), were also tested and showed similar increased expression upon HDE + CO2 exposure. A chemokine array analysis of BAL fluid revealed that MIP-1γ (CCL9) shows a similar increased response to HDE + CO2. Further testing showed CCL9 was significantly elevated by barn dust and further enhanced by CO2 co-exposure in a dose-dependent manner that was noticeable at the protein and mRNA levels. In all cases, except for ICAM-1, increases in tested markers in the presence of elevated CO2 were only significant in the presence of HDE as well. CONCLUSIONS: We show that even at mandated safe exposure limits, CO2 is capable of enhancing multiple markers of inflammation in response to HDE

Effect of low-level CO2 on innate inflammatory protein response to organic dust from swine confinement barns.

BACKGROUND: Organic hog barn dust (HDE) exposure induces lung inflammation and long-term decreases in lung function in agricultural workers. While concentrations of common gasses in confined animal facilities are well characterized, few studies have been done addressing if exposure to elevated barn gasses impacts the lung immune response to organic dusts. Given the well documented effects of hypercapnia at much higher levels we hypothesized that CO2 at 8 h exposure limit levels (5000 ppm) could alter innate immune responses to HDE. METHODS: Using a mouse model, C57BL/6 mice were nasally instilled with defined barn dust extracts and then housed in an exposure box maintained at one of several CO2 levels for six hours. Bronchiolar lavage (BAL) was tested for several cytokines while lung tissue was saved for mRNA purification and immunohistochemistry. RESULTS: Exposure to elevated CO2 significantly increased the expression of pro-inflammatory markers, IL-6 and KC, in BAL fluid as compared to dust exposure alone. Expression of other pro-inflammatory markers, such as ICAM-1 and matrix metalloproteinase-9 (MMP-9), were also tested and showed similar increased expression upon HDE + CO2 exposure. A chemokine array analysis of BAL fluid revealed that MIP-1γ (CCL9) shows a similar increased response to HDE + CO2. Further testing showed CCL9 was significantly elevated by barn dust and further enhanced by CO2 co-exposure in a dose-dependent manner that was noticeable at the protein and mRNA levels. In all cases, except for ICAM-1, increases in tested markers in the presence of elevated CO2 were only significant in the presence of HDE as well. CONCLUSIONS: We show that even at mandated safe exposure limits, CO2 is capable of enhancing multiple markers of inflammation in response to HDE

RNA expression of TLR10 in normal equine tissues

Background: Toll like receptors are one of the major innate immune system pathogen recognition systems. There is little data on the expression of the TLR10 member of this family in the horse. Results: This paper describes the genetic structure of the Equine TLR10 gene and its RNA expression in a range of horse tissues. It describes the phylogenetic analysis of the Equine TLR1,6,10,2 annotations in the horse genome, firmly identifying them in their corresponding gene clades compared to other species and firmly placing the horse gene with other TLR10 genes from odd-toed ungulates. Additional 3’ transcript extensions to that annotated for TLR10 in the horse genome have been identified by analysis of RNAseq data. RNA expression of the equine TLR10 gene was highest in peripheral blood mononucleocytes and lymphoid tissue (lymph nodes and spleen), however some expression was detected in all tissues tested (jejunum, caudal mesenteric lymph nodes, bronchial lymph node, spleen, lung, colon, kidney and liver). Additional data on RNAseq expression of all equine TLR genes (1–4 and 6–10) demonstrate higher expression of TLR4 than other equine TLRs in all tissues. Conclusion: The equine TLR10 gene displays significant homology to other mammalian TLR10 genes and could be reasonably assumed to have similar fuctions. Its RNA level expression is higher in resting state PBMCs in horses than in other tissues

Comparing techniques for determining steer diets in northern Chihuahuan Desert

Diets determined by bite count and microhistological analysis of esophageal extrusa and feces were compared for steers grazing on grass-shrublands in the northern Chihuahuan Desert. The study was conducted on the Chihuahuan Desert Rangeland Research Center near Las Cruces, New Mexico. The purpose was to determine the similarity of 3 dietary techniques on arid, heterogeneous rangeland. It was proposed that the number of bites of each species eaten was directly proportional to the weight eaten as determined by the 2 microhistological techniques. Samples of diets were collected in 4 seasons from 2 steers grazing in a continuous yearlong pasture and in season-long rotation pastures. The 3 dietary techniques did not give similar (P<0.10) estimates of the diets eaten by the steers. Mean similarity indices were highest (77%) comparing diets from analysis of esophageal and fecal material. Lowest mean similarity indices (57%) were from comparing diets from bite count and fecal analysis. Much of the discrepancy between techniques was because of different size plants being eaten and heterogeneity of plant distribution. An importance ranking of dietary species using the 3 techniques showed that the top 3 species comprised over 68% of the total diets. Any of the 3 techniques can be used to determine the common species in the diets which may be all that is necessary for some management and analysis needs.The Journal of Range Management archives are made available by the Society for Range Management and the University of Arizona Libraries. Contact [email protected] for further information.Migrated from OJS platform August 202

Organic barn dust inhibits surfactant protein D production through protein kinase-c alpha dependent increase of GPR116.

Prolonged exposure to organic barn dusts can lead to chronic inflammation and a broad range of lung problems over time, mediated by innate immune mechanisms. The immune surfactant or collectin surfactant protein D (SP-D) is a crucial multifunctional innate immune receptor. Little work to date has examined the effect of such collectins in response to organic dusts. We provide evidence here that agricultural organic dusts can inhibit mRNA and protein expression of SP-D in a human alveolar epithelial cell line, and an in vivo mouse model. This inhibition was not a result of lipopolysaccharide (LPS) or peptidoglycans, the two most commonly cited immune active components of these dusts. We further show that inhibition of the signaling molecule protein kinase C alpha (PKCα) can reverse this inhibition implicating it as a mechanism of SP-D inhibition. Examination of the SP-D regulatory receptor GPR116 showed that its mRNA expression was increased in response to dust and inhibited by blocking PKCα, implicating it as a means of inhibiting SP-D in the lungs in response to organic dusts. This reduction shows that organic barn dust can reduce lung SP-D, thus leaving workers potentially at risk for a host of pathogens

Influence of saline water on intake, digesta kinetics, and serum profiles of steers

Nine yearling Holstein steers (avg weight 234 kg) were used to evaluate the influence of water salinity on feed and water intake, as well as several ruminal and serum characteristics. The ruminally cannulated steers were individually fed low-quality mixed hay simulating a range diet. Steers were assigned randomly to receive either control (C) water containing 350 ppm total dissolved solids (TDS) or a treated water (HS) containing 2,300 ppm TDS. The experiment included a 14-day adjustment period and a 15-day measurement period. High-saline water did not affect (P = 0.18) feed or water intake, although there was a tendency for greater consumption of both feed and water in HS steers. The HS steers had slower (P = 0.10) particulate passage rates and longer (P = 0.06) rumen retention times on day 1 of the measurement period, indicating possible differences in particle density and (or) particle size. On day 1, undigested dry matter (DM) fill was greater (P = 0.05) in HS steers compared with C (80.7 vs 61.5 g/kg BW); similar trends occurred on day 8. The HS steers also had greater (P = 0.02) rumen fluid volumes, but similar (P = 0.45) fluid dilution rates compared with C steers. No in situ DM disappearance differences were detected (P greater than or equal to 0.38) at incubation times ranging from 12 to 72 hours. No clinical or sub-clinical toxicological symptoms were observed in HS compared with C steers. This study suggests that cattle can ingest saline water containing 2,300 ppm TDS on a short-term basis with no adverse effects.This material was digitized as part of a cooperative project between the Society for Range Management and the University of Arizona Libraries.The Journal of Range Management archives are made available by the Society for Range Management and the University of Arizona Libraries. Contact [email protected] for further information.Migrated from OJS platform August 202