[Nematode infections in mice--an experimental model of immunoregulation]. / Zarazenia nicieniami u myszy--eksperymentalny model immunoregulacji.

There has been a substantial increase in the incidence of autoimmune and allergic diseases in Western countries in the past few decades. However, in the geographic area endemic for parasitic helminth infections, such diseases remain relatively rare. It has been hypothesized that helminths may protect against immune disorders that have been observed in urbanized area. Studies on rodents infected with nematodes Trichinella spiralis, Heligmosomoides polygyrus, Nippostrongylus brasiliensis and Trichuris muris have provided considerable information about immune mechanisms in aspects of host-parasite interaction and immunoregulation. Helminths inducing a long-lasting asymptomatic infection are regarded as major modifiers of the host immune system. Parasitic worms can establish and reproduce in mammalian hosts switching off inflammation and inducing a tolerant response to parasitic antigens. In this review we summarized recent information on the immunoregulation during nematode infection and mechanisms used by nematodes, including the induction of regulatory T cells and apoptosis in the host. The innate immune response seems to determine the different sensitivity of mice to nematode infection. In this review we also discuss results of our own studies on H. polygyrus, demonstrating that it induces different mechanisms in different strains of mice which might play important role in the modulation of immune response. In the slow responder mice apoptosis would play a key role in the outcome of immune response. Contrary to that, in fast responder mice a defensive inflammatory response is mostly down-regulated via endogenous opioids pathway. Understanding the molecular mechanisms that mediate the effects that helminths have on the immune system will provide information that can be exploited to prevent inflammatory diseases.

Heligmosomoides polygyrus: opioid peptides are involved in immune regulation of the histotropic phase of infection.

We investigated the potential effect of agonists of opioid receptors in the experimental model of Heligmosomoides polygyrus primary infection. BALB/c mice infected with H. polygyrus were treated with naltrexone, a non-specific antagonist of all three types of opioid receptors (mu, delta, kappa) prior to and during infection. The blockade of opioid receptors affected the pattern and level of immune response induced by H. polygyrus in the histotropic phase of infection, which suggests that an opioid receptor-linked mechanism is involved in the immune response of mice during this phase of infection. Down-regulation of the inflammatory response against fourth-stage larvae appeared to be by endogenous opioids influenced cytokines and nitric oxide production by macrophages in the peritoneum and in the gut as well as migration of leukocytes towards the antigens. Down-regulation of these mechanisms by opioid receptor agonists in vivo might account for the decreased resistance to H. polygyrus infection.

[Apoptosis, a protective mechanism for pathogens and their hosts]. / Apoptoza jako mechanizm ochronny dla patogenów i ich zywicieli.

In this review we summarize the great amount of recent information on the apoptosis in aspects of the host-parasite interaction. Although apoptosis is a form of programmed cell death which plays a pivotal role in normal tissue development a plethora of pathogens including parasitic protista and helminths are able to modulate host apoptosis pathways to their own advantage. Here in we present and discuss new research data and results describing the phenomenon as a process have been controlled by gene expression, biochemical reactions and receptor-ligand interactions at the cell membrane surface. Section 1 describes apoptosis as ongoing process in normal tissue development. Section 2 analyzes the role of apoptosis in outcome of infection and pathogenesis of several disorders evoked by viruses and bacteria. The cellular mechanisms of cell death during infection with unicellular parasites such as Leishmania sp. and Plasmodium sp. are described in Section 3. In the next paragraph the potency of parasitic protista and helmiths for modulation host apoptosis pathways to their own advantage is discussed. The involvement of apoptosis in immunoregulation of the host immune function was proposed as a one of possible mechanism in creation of the host-parasite relationship. The molecular and cellular mechanisms of parasite-induced immune response via apoptosis pathways are discussed. We conclude that novel strategies for the management of the host-parasite relationships need to be explained into the mechanisms by which parasites induced apoptosis in contribution to the activity of immune system of the host.