Role of intestinal epithelial cells in the innate immune defence of the pig intestine

The intestinal epithelium serves as a dynamic barrier, which in the course of its normal function, maintains regulated uptake of nutrients and water while excluding potential pathogens. Over the past decade many studies have also revealed the immunological importance of intestinal epithelial cells (IEC). IEC have developed a variety of mechanisms to reduce the risk of infection by invasive pathogens or damage by toxic compounds. The effective maintenance of a physical barrier function is dependent on the establishment of well-organised intercellular junctions and a constant state of regeneration/renewal of the epithelium. IEC also participate in the innate immune responsiveness of the intestine by their ability to secrete mucus and antimicrobial peptides. IEC are also able to secrete cytokines and to respond to exogenous chemokines. This review summarises the current knowledge of the innate immune mechanisms developed by porcine IEC.     

免疫系统乃霉菌毒素攻击的目标——霉菌毒素损害猪的健康

霉菌毒素是由生长在动物饲料和人类食品上的真菌所产生的结构各异的二级代谢产物.动物摄入中等至高剂量霉菌毒素引起的临床中毒综合征已有详细描述.     

Nitrous oxide emission from herbicide-treated soybean

 The emission of N₂O from soybean plants treated with the herbicides dichlorophenoxyacetic acid (2,4-D) and bromoxynil was studied. The N₂O flux from 2,4-D- and bromoxynil-treated soybean was 14.1 ng N₂O-N g^–1 fresh weight h^–1 and 19.7 ng N₂O-N g^–1 fresh weight h^–1, respectively, i.e. approximately twice that of the controls. The NO₂ ^–-N concentration in 2,4-D- and in bromoxynil-treated soybean was about 8 μg N g^–1 fresh weight, i.e. fivefold the concentration found in control plants. The NO₃ ^– content in herbicide-treated soybean did not differ significantly from that of the control plants. Consequently, the accumulation of NO₂ ^–-N during the assimilation of NO₃ ^–-N was thought to cause the observed N₂O release. Probably, N₂O is a by-product produced during either the reaction of NO₂ ^–-N with plant metabolites or NO₂ ^–-N decomposition. Final conclusions must await further experiments. Received: 5 November 1999     

The Effect of Different Shade Levels on Growth and Tuber Yield of Sweet Potato: II. Tuber Yield

Eight sweet potato cultivars ( Ipomoea batatas Lam.) were grown under four different light regimes (0, 26, 42 and 60 % light reduction (LR)) at two experimental sites of the International Potato Center (CIP) in Peru during the 1990 and 1991 growing season. Increasing shade diminished the tuber yield of five cultivars, two showed a tolerance for slight (26 % LR) and moderate (42 % LR) shade and one had the same yield in full sunshine and slight shade. Shade mainly reduced the sink-size (tubers m ⁻²) of sweet potato and to a lesser extent the sink-strength. The growth of the plant top was hardly affected by shade; slight shade even favoured shoot development of some cultivars. The plant top was the stronger sink under shade conditions and tuber yield was not only reduced by lesser assimilate production as a whole but also by an altered assimilate partitioning.     

The use of asulam to control Bromus sterilis in ryegrass crops grown for seed

Asulam applied in April 1981 and 1982 gave good control of established plants of Bromus sterilis growing in Italian and perennial ryegrass crops grown for seed. Doses of 1–3 kg a.i./ha reduced numbers of weed inflorescences by 65–90%. The results also showed that there was no effect on crop heading and further suggested that seed yield had not been reduced. Two pot experiments also indicated the efficacy of asulam at 0·5-2 kg a.i./ha applied pre-emergence and further study of such treatment in the autumn during the establishment of a ryegrass seed crop is warranted.     

The fungal T-2 toxin alters the activation of primary macrophages induced by TLR-agonists resulting in a decrease of the inflammatory response in the pig

T-2 toxin is known to be one of the most toxic trichothecene mycotoxins. Exposure to T-2 toxin induces many hematologic and immunotoxic disorders and is involved in immuno-modulation of the innate immune response. The objective of this work was to evaluate the effects of T-2 toxin on the activation of macrophages by different agonists of Toll-like receptors (TLR) using an in vitro model of primary porcine alveolar macrophages (PAM). Cytotoxic effects of T-2 toxin on PAM were first evaluated. An IC₅₀ of 19.47 ± 0.9753 nM was determined for the cytotoxicity of T-2 toxin. A working concentration of 3 nM of T-2 toxin was chosen to test the effect of T-2 toxin on TLR activation; this dose was not cytotoxic and did not induce apoptosis as demonstrated by Annexin/PI staining. A pre-exposure of macrophages to 3 nM of T-2 toxin decreased the production of inflammatory mediators (IL-1 beta, TNF-alpha, nitric oxide) in response to LPS and FSL1, TLR4 and TLR2/6 agonists respectively. The decrease of the pro-inflammatory response is associated with a decrease of TLR mRNA expression. By contrast, the activation of TLR7 by ssRNA was not modulated by T-2 toxin pre-treatment. In conclusion, our results suggest that ingestion of low concentrations of T-2 toxin affects the TLR activation by decreasing pattern recognition of pathogens and thus interferes with initiation of inflammatory immune response against bacteria and viruses. Consequently, mycotoxins could increase the susceptibility of humans and animals to infectious diseases.     

The food contaminant fumonisin B1 reduces the maturation of porcine CD11R1+ intestinal antigen presenting cells and antigen-specific immune responses, leading to a prolonged intestinal ETEC infection

Consumption of food or feed contaminated with fumonisin B₁ (FB₁), a mycotoxin produced by Fusarium verticillioides, can lead to disease in humans and animals. The present study was conducted to examine the effect of FB₁ intake on the intestinal immune system. Piglets were used as a target and as a model species for humans since their gastro-intestinal tract is very similar. The animals were orally exposed to a low dose of FB₁ (1 mg/kg body weight FB₁) for 10 days which did not result in clinical signs. However, when compared to non-exposed animals, FB₁-exposed animals showed a longer shedding of F4⁺ enterotoxigenic Escherichia coli (ETEC) following infection and a lower induction of the antigen-specific immune response following oral immunization. Further analyses to elucidate the mechanisms behind these observations revealed a reduced intestinal expression of IL-12p40, an impaired function of intestinal antigen presenting cells (APC), with decreased upregulation of Major Histocompatibility Complex Class II molecule (MHC-II) and reduced T cell stimulatory capacity upon stimulation. Taken together, these results indicate an FB₁-mediated reduction of in vivo APC maturation.     

The effects of mycotoxins, fungal food contaminants, on the intestinal epithelial cell-derived innate immune response

Mycotoxins are structurally diverse fungal metabolites that can contaminate a variety of dietary components consumed by animals and humans. It is considered that 25% of the world crop production is contaminated by mycotoxins. The clinical toxicological syndromes caused by ingestion of moderate to high amounts of mycotoxins and their effect on the immune system have been well characterized. However, no particular attention has been focused on the effects of mycotoxins on the local intestinal immune response. Because of their location, intestinal epithelial cells (IECs) could be exposed to high doses of mycotoxins. As a component of the innate local immune response, intestinal epithelial cells have developed a variety of mechanisms which act to reduce the risk of infection by microorganisms or intoxication by toxic compounds. This review summarises the innate immune response developed by intestinal epithelial cells and reports the literature concerning the effects of mycotoxins on them. Particularly, the effects of mycotoxins on the maintenance of a physical barrier by epithelial cells will be discussed together with their effect on extrinsic protective components of the innate intestinal immunity: mucus secretion, antimicrobial peptide generation, IgA and pro-inflammatory cytokine release.