Differential expression of intestinal genes in necrotic enteritis challenged broiler chickens with 2 different Clostridium perfringens strains

Abstract

The primary cause of necrotic enteritis ( NE ) disease in chickens is the NetB-positive Clostridium perfringens bacterium. Many factors are known to affect the severity of NE in the challenge models of broiler chickens, and one of these factors is the virulence of C. perfringens strain. This study was conducted to evaluate the effect of 2 pathogenic C. perfringens strains in a NE challenge model on gut health and mRNA expression of genes encoding apoptosis, tight junction, immunity, and nutrient transporters in broilers. Day-old Ross-308 male broilers ( n = 468) were allocated in a 2 × 3 factorial arrangement of treatments with in-feed antibiotics (no or yes) and challenge (Non, C. perfringens strain NE18, and C. perfringens strain NE36) as the factors. The birds in the challenged groups were inoculated with Eimeria species on day 9 and with a fresh suspension of C. perfringens NE18 or NE36 on day 14 and 15. Sample collection was performed on 2 birds of each pen on day 16. Necrotic enteritis challenge, impaired feed conversion ratio during day 0 to 16 compared with the control group where the effect of the NE36 challenge was more severe than that with NE18 ( P < 0.001). The mRNA expression of mucin-2, immunoglobulin-G, occludin ( P < 0.001), and tight junction protein-1 ( P < 0.05) genes were downregulated in both challenged groups compared with the nonchallenged counterparts. Antibiotic supplementation, on the other hand, increased weight gain, and feed intake in all challenged birds ( P < 0.01), but upregulated mucin-5ac and alanine, serine, cysteine, and threonine transporter-1 ( P < 0.05) only in the NE18 challenged birds. The challenge with NE36 significantly upregulated caspase-8 and claudin-1 ( P < 0.001), but downregulated glucose transporter-2 ( P < 0.001) compared with the NE18 challenge. These results suggest that NE challenge is detrimental to the performance of broilers through compromised intestinal health, and different C. perfringens strains can affect the severity of the disease through modulating the expression of intestinal genes encoding proteins responsible for apoptosis, gut integrity, immunity, mucus production, and nutrient transporters.

A Microencapsulated Mixture of Eugenol and Garlic Tincture Supplementation Mitigates the Effect of Necrotic Enteritis on Intestinal Integrity and Increases Goblet Cells in Broilers

“…The results observed in the current study showed that NE challenge downregulated OCLN in male birds and MUC2 in both male and female birds. These results were consistent with previous findings in broilers where birds challenged with NE had downregulated OCLN genes [ 41 ]. Interestingly, CLDN1 and JAM2 were upregulated by NE challenge, and it is contrary to their function as tight junction proteins.…”

“…Interestingly, CLDN1 and JAM2 were upregulated by NE challenge, and it is contrary to their function as tight junction proteins. However, as discussed by Gharib-Naseri et al [ 41 ], the upregulation of CLDN1 may not be an indication of better tight junction function but other mechanisms may be involved. Therefore, we speculate that it may not be a good marker for the indication of gut integrity at least in the NE challenge studies.…”

Monoglyceride Blend Reduces Mortality, Improves Nutrient Digestibility, and Intestinal Health in Broilers Subjected to Clinical Necrotic Enteritis Challenge

“…Wang et al [59] confirmed the significant effect of NE on immunoglobulin genes evidenced by the reduced expression of IgA+ B cells in birds infected with NE. Similarly, Gharib-Naseri et al [35] reported a reduced expression of IgG and IgM genes in NE challenged birds. In the current study, upregulation of IgG gene in birds fed MG and MGFA compared to the NC group indicates that the birds fed additives had a greater immune response.…”

“…The expression of TJP1 gene is correlated with other tight junction genes in the epithelium [52]. Enteric diseases such as NE damage intestinal integrity and downregulates tight junction gene expression (CLDN, OCLN, and TJP1), resulting in increased intestinal permeability [35,53,54]. However, it should be noted that damage in the intestinal epithelium and disturbances in the function of genes regulating tight junctions and immunity can be due to the Eimeria-caused infections prior to C. perfringens challenge of the birds.…”

Structural Changes in Trabecular Bone, Cortical Bone and Hyaline Cartilage as Well as Disturbances in Bone Metabolism and Mineralization in an Animal Model of Secondary Osteoporosis in Clostridium perfringens Infection

“…All these indicate that broiler chickens can be used to study the effect of disturbances in the gastrointestinal microflora, which in turn significantly affect the absorption of nutrients [ 20 ]. Numerous recent studies showed changes in gene expression of proteins are responsible for intestinal tight junction integrity or barrier function (claudin-1, occludin, mucin-2, Fatty acid-binding protein-2) in broiler chickens during gut inflammation induced by C. perfringens challenge, which are similar to those observed in humans during the IBD [ 47 , 48 , 49 , 50 ]. Broiler chickens are also sensitive to C. perfringens , which facilitated the infection process itself.…”