Preexisting Trichinella spiralis infection attenuates the severity of Pseudomonas aeruginosa-induced pneumonia

Abstract

Background A range of helminth species involve the migration of developing larvae through the lung and establish chronic infections in the host that include potent immune regulatory effects. Trichinella spiralis is one of the most successful parasitic symbiotes. After released by intestinal female adult worms, newborn larvae of T. spiralis travel through the circulatory system to the lung and finally reach skeletal muscle cells. As unique inflammation modulator of intracellular parasitism, T. spiralis shows improved responses to autoimmune disease and viral pulmonary inflammation by exerting immunomodulatory effects on innate and adaptive immune cells. Methodology/Principal findings C57BL/6 mice were divided into four groups: uninfected; helminth- T. spiralis infected; P. aeruginosa infected; and co-infected. Mice infected with T. spiralis were incubated for 6 weeks, followed by P. aeruginosa intranasal inoculation. Bronchial alveolar lavage fluid, blood and lung samples were analyzed. We found that T. spiralis induced Th2 response in the mouse lung tissue, increased lung CD4+ T cells, GATA3, IL-4, IL-5 and IL-13 expression. Pre-existing T. spiralis infection decreased lung neutrophil recruitment, inflammatory mediator IL-1β and IL-6 expression and chemokine CXCL1 and CXCL2 release during P. aeruginosa- pneumonia. Furthermore, T. spiralis co-infected mice exhibited significantly more eosinophils at 6 hours following P. aeruginosa infection, ameliorated pulmonary inflammation and improved survival in P. aeruginosa pneumonia. Conclusions These findings indicate that a prior infection with T. spiralis ameliorates experimental pulmonary inflammation and improves survival in P. aeruginosa pneumonia through a Th2-type response with eosinophils.

The gut microbiota is essential forTrichinella spiralis- evoked suppression of colitis

“…Humans contract T. spiralis by consuming uncooked meat that carries encysted T. spiralis larvae in muscle tissue; then larvae are released by gastric fluids, molt and mature into adult worm. The female adult worms release newborn larvae after copulation, which travel through the circulatory system to reach skeletal muscle cells [14, 15]. As a helminth with all stages of larval and adult development occurring within the same host organism, T. spiralis is one of the most successful parasitic symbiotes, ensuring its survival and immune dialogue with the host [16].…”

“…Results then larvae are released by gastric fluids, molt and mature into adult worm. The female adult worms release newborn larvae after copulation, which travel through the circulatory system to reach skeletal muscle cells [14,15]. As a helminth with all stages of larval and adult development occurring within the same host organism, T.…”

“…spiralis can mediate protection against allergic asthma, Pseudomonas aeruginosainduced pneumonia, influenza or respiratory syncytial virus-associated pathologies in mice [15,[17][18][19]. Evidence also indicates that T. spiralis infection attenuates…”

Appraisal of Chitosan-Coated Lipid Nano-Combination with Miltefosine and Albendazole in the Treatment of Murine Trichinellosis: Experimental Study with Evaluation of Immunological and Immunohistochemical Parameters

“…Expression of GATA3 in the positive control group was significantly enhanced either in intestinal or muscular phases than in the negative control group; these results agreed with Long et al . [ 54 ], as T . spiralis induced Th2 response in the mouse lung tissue, increased lung CD4 + T cells, GATA3, IL-4, IL-5, and IL-13 expression.…”

The impact of helminth-induced immunity on infection with bacteria or viruses

“…H. polygyrus infection also can enhance acute airway neutrophil responses to P. aeruginosa infection to improve survival rates [ 50 ]. In addition, prior infection with Trichinella spiralis improved pulmonary inflammation and survival after P. aeruginosa infection and pneumonia through a T H 2-type response associated with eosinophils [ 51 ]. Helminth infections result in the recruitment of eosinophils that supports persistence and survival by limiting the development of tissue-destructive T H 1-type immune responses [ 52 ].…”