Piscine mast cells or eosinophilic granule cells (EGCs) of fish are equivalent to the mammalian mast cells. Recently, a better understanding of EGCs functions is allowed because of the growing interest in fish models. Herein, we present a trial to furnish data regarding the distribution of the EGCs in the fish olfactory organ, an issue that has not been reported so far. Regarding their distribution, two kinds of EGCs had been identified. An intra-epithelial one was detected in the olfactory epithelium lining of the olfactory lamellae. The stromal one was identified in the connective tissue core of the olfactory lamellae and in the lamina propria underlying the olfactory epithelium. Some were detected in the capillary lumen. The cytoplasm of the EGCs reacted strongly with the MMP-9 antibody. Stimulating a migration perspective for the olfactory EGCs which was confirmed by their location in the blood capillaries. Several EGCs could be verified in close relation, some underneath the epineurium, with the nerve fiber. Mutually, this verifies the existence of intra-epithelial and stromal migrating EGCs in the catfish olfactory organ and their inclusion in the olfactory immune response. Additionally, this provides evidence for an immune–nervous interaction to influence both the immune reactions and the nervous scheme in catfish.

Galectins are a family of proteins that bind β-galactosides and play key roles in a variety of cellular processes including host defence. They have been well studied in hosts but less so in gastrointestinal nematodes. Both host and parasite galectins are present in the gastrointestinal tract following infection. Parasite galectins can both bind antibody, especially highly glycosylated IgE and be bound by antibody. Parasite galectins may act as molecular sponges that soak up antibody. Host galectins promote mast cell degranulation while parasite galectins inhibit degranulation. Host and parasite galectins can also bind mucins and influence mucus viscosity. As the protective response against gastrointestinal nematode infection is partly dependent on IgE mediated mast cell degranulation and mucus, the interactions between host and parasite galectins play key roles in determining the outcome of infection.

Mast cells (MCs) are granulated cells of haematopoietic lineage and constitute a major sensory arm of the immune system. MCs dually guard hosts and regulate immune responses against invading pathogens. This property of the MCs is attributed to their adaptability to detect stress signals and pathogens, and the production of signal specific mediators to engage immune cells for clearance of infectious agents. Pathogen-specific signals establish basis for the initiation of adoptive immune responses. These immune regulatory roles of MCs have opened avenues to engage different MCs activators which culminate in effective passive immunisation. The molecular mechanisms and dynamics of functionalities of MCs in host defences have been extensively characterised in mammals and rodents, and research on MCs in avian species is emerging. This review surveys the development, morphology and distribution of MCs in different tissues of the poultry and highlight areas that can be exploited for disease control and prevention.

The complexity of helminth macroparasites is reflected in the intricate network of host cell types that participate in the Type 2 immune response needed to battle these organisms. In this context, adaptive T helper 2 cells and the Type 2 cytokines interleukin (IL)-4, IL-5, IL-9 and IL-13 have been the focus of research for years, but recent work has demonstrated that the innate immune system plays an essential role. Some innate immune cells that promote Type 2 immunity are relatively abundant, such as macrophages and eosinophils. However, we now appreciate that more rare cell types including group 2 innate lymphoid cells, basophils, mast cells and dendritic cells make significant contributions to these responses. These cells are found at low frequency but they are specialized to their roles – located at sites such as the skin, lung and gut, where the host combats helminth parasites. These cells respond rapidly and robustly to worm antigens and worm-induced damage to produce essential cytokines, chemokines, eicosanoids and histamine to activate damaged epithelium and to recruit other effectors. Thus, a greater understanding of how these cells operate is essential to understand how the host protects itself during helminth infection.

Acupuncture has been in clinical practice in China for thousands of years and its analgesia effect is worldwide accepted. However, the mechanism of acupuncture effect is not well understood. The study focus on signaling pathways induced by acupuncture, analyzes the cooperative action of the acupoints’ structure and the associated chemical mediators during acupuncture, establishes a mathematical model clarifying the roadmap of electroneurographic signal startup and transmission mechanism induced by acupuncture, quantitatively analyzing the response in acupoints to acupuncture. These work contribute to reveal the activation and transmission mechanism of neural signals induced by acupuncture from systems biology perspective, lay the foundation for the integration of acupuncture theory and modern science and further guide the clinical treatment and experimental research of acupuncture.

Previous studies have shown that host immunity regulates the fecundity of nematodes. The present study was aimed at clarifying the reversible nature of fecundity in response to changes of immunological status and to determine which effector cells are responsible for compromising fecundity in Heligmosomoides polygyrus. Enhanced fecundity was observed in immunocompromised SCID and nu/nu mice compared to those in the corresponding wild-type mice, with significantly fewer numbers of intrauterine eggs produced in the wild-type than in the immunodeficient mice. When 14-day-old adult worms from BALB/c mice were transplanted into naïve BALB/c mice, their fecundity increased significantly as early as 24 h post-transplantation, but not when they were transferred into immune mice, suggesting the plastic and reversible nature of fecundity in response to changes in host immunological status. In mast cell-deficient W/Wv mice, nematode fecundity was significantly higher than in mast cell-reconstituted W/Wv or +/+ mice. The serum levels of the mast-cell protease mMCP1 were markedly increased in the wild-type as well as the mast cell-reconstituted W/Wv, but not in the W/Wv, SCID, or nu/nu mice during infection. These findings raise the interesting possibility that certain activities of mast cells, either directly or indirectly, regulate parasite fecundity during infection.

Adults of the porocephalid pentastomid Porocephalus crotali infect the lung of rattlesnake definitive hosts and larvae develop in rat intermediate hosts. In the latter, nymphs encyst within a variety of tissue sites (commonly abdominal fat bodies and lungs) and each becomes the focus of an eosinophilic granuloma. From an early stage in infections, granulomas become increasingly infiltrated by mast cells which, using conventional histology and paired immunofluorescence against mast cell proteases, appear to be exclusively of the mucosal phenotype. Mucosal mast cells are concentrated along the dorsal region of the parasite and in a plug of tissue containing degenerating cuticles within independent granulomas, which is located between its head and tail. ELISAs against the rat mast cell proteases I and II (RMCP I and II), extracted from abdominal fat, lung, spleen, liver and kidney granulomas at various intervals post-infection, reveal a substantially elevated concentration of RMCP II in all lesions. In fat, concentrations increase up to about 100 days post-infection, at which time moulting ceases and inflammatory responses subside. RMCP II was scarcely detectable in matched control tissues. Unlike infections with certain nematode parasites, where enteric mucosal mast cells secrete RMCP II systemically, concentrations of RMCP II in the serum of infected rats were significantly reduced when compared with age-matched uninfected controls. These results confirm that P. crotali can selectively recruit mucosal mast cells to a variety of tissue sites, most of which are non-mucosal. Possible mechanisms are discussed.

Mast cells of connective tissue type are scattered in the interstitial compartment of the lizard Podarcis s. sicula. Their number varies during the year, showing peaks in spring and in winter, respectively.Thermal manipulation affects mast cell number (MCN): high temperature decreased MCN in both January and May, while low temperature increased MCN only in January. Ethane dimethane sulphonate, a toxin which specifically destroys Leydig cells, induced an increase in MCN on days 3 and 7 of treatment. Oestradiol treatment provoked a strong increase in MCN that was blocked by tamoxifen. Blocking androgen receptors with cyproterone acetate resulted in an increase in MCN, while testosterone injection provoked a strong decrease. These results suggest a relationship between the presence of mature Leydig cells and mast cell proliferation and/or differentiation.

This study compared the immunological and biochemical responses of co-grazed Suffolk and Texel lambs to a natural gastrointestinal nematode infection. Variables analysed included serum pepsinogen, total protein, albumin, haematological variables and nematode-specific serum immunoglobulin activity, at 11, 14 and 17 weeks of age. At 17 weeks, randomly selected lambs were necropsied to determine worm burdens, nematode-specific mucosal abomasal and intestinal immunoglobulin activity. Nematode burden, faecal egg count and pepsinogen concentrations were significantly higher in Suffolks relative to Texels, at all 3 time-points investigated. Suffolks displayed significantly higher erythrocyte, total leukocyte, lymphocyte and neutrophil counts, mean cell volume and packed cell volume, than Texels (P<0·01). However, breed differences in eosinophil counts were not significant. While serum nematode-specific antibody activity levels were significantly higher (P<0·001) in Texels for all isotypes measured, antibody activity levels at a mucosal level were equivalent in both breeds. Correlation analysis of mucosal antibody levels and nematode variables highlighted a more consistent pattern of events in Texels, with more mucosal antibodies negatively correlated with FEC and worm burden, in comparison to Suffolks. In particular, an important role for mucosal IgE is proposed. In Texels, a significant and negative correlation was identified between IgE and faecal egg counts and worm burden (FEC: −0·48, P<0·005). This was not observed in Suffolks. The evidence suggests that susceptibility in Suffolks may be mediated through poor IgE affinity/avidity and/or through deficiencies in related mechanisms such as mast cell production, recruitment or activation.

It has been reported that infection with Nippostrongylus brasiliensis induces villus atrophy with various histological alterations. In N. brasiliensis-infected rats, villus length in the jejunum was reduced significantly at day 10 p.i., when serum levels of rat mast cell protease (RMCP) II had increased significantly. To determine whether the villus atrophy is associated with enhancement of apoptosis, apoptotic nuclei were labelled using the nick end-labelling method. Numbers of labelled cells were markedly increased in the villus epithelium at 7–10 days p.i., while the numbers returned to normal 14 days p.i. when worms were rejected from the intestine and villus length became normal. Examination of the expression of the adhesion molecule E-cadherin showed granular immunoreactivity in the cytoplasm of atrophic villus epithelium with loss of normal localization to epithelial cell borders. In mast cell-deficient Ws/Ws rats, villus length was reduced as significantly as in +/+ counterparts at day 10 p.i. with marked increases in the numbers of apoptotic cells. These results suggested that villus atrophy was closely associated with enhanced apoptosis and loss of adhesion in epithelial cells. Mast cell activation appears not to be involved in these alterations.

The time-course of differentiation/proliferation of mast cells in gut epithelium was investigated in mice infected with the nematode Strongyloides venezuelensis. After infection, expression of proliferating cell nuclear antigen increased in gut intraepithelial mast cells on days 7 to 11, followed by an increase in the number of intraepithelial mast cells from days 11 to 14. Mast cell precursors were defined as cells that formed mast cell colonies in methylcellulose culture. After infection, the numbers of mast cell precursors in the population of gut intraepithelial mononuclear cells (IEMNC) increased significantly on day 3 and returned to the pre-infection level by day 7. Mast cell precursors in Peyer's patches, mesenteric lymph nodes (MLN), and spleen also increased from day 7 p.i. Production of IL-3 and IL-4 in MLN and spleen were increased between 7 and 11 days p.i. These results show that murine intestinal mastocytosis is initiated by an early increase in mast cell precursor number in the gut epithelium followed by proliferation/differentiation of mast cells. Mast cell precursor numbers increased even before the production of IL-3 and IL-4 in MLN and spleen, suggesting that some local factors might be involved in this phenomenon.

The ultrastructure of mast cells from the nine normal inferior turbinates were compared with those found in eight patients with perennial allergic rhinitis due to house dust mite allergy. Forty-six mast cells from normal patients were found in forty blocks and eighty cells were found in thirty-three blocks in patients with perennial allergy suggesting an increase of mast cell numbers in perennial allergy. There were no basophils outside the blood vessels and whole mast cells were found only in the submucosa. There was no difference in the morphology of cells of different sizes. Mast cells were more degranulated in the allergic mucosa. Degranulation, irrespective of cell size was found at all depths of the mucosa. A review of the literature covered the in vivo and in vitro descriptions of the ultrastructural morphology of human mast cells in the respiratory tract.