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Background. To investigate the climb stairs resistance exercise on nociception and axonal regeneration in the sciatic nerve of rats. Methods. 24 Wistar rats were divided: control group (CG—no injury), exercise group (EG—no injury with physical exercise), lesion group (LG—injury, but without exercise), and treated group (LEG—injury and physical exercise). LG and LEG were subjected to sciatic nerve compression with hemostat. From the 3rd day after injury began treatment with exercise, and after 22 days occurs the removal of a nerve fragment for morphological analysis. Results. Regarding allodynia, CG obtained values less than EG (p=0.012) and larger than LG and LEG (p

The longitudinal growth of long bones is attributed to epiphyseal growth. However, the effects of low-level laser therapy (LLLT) in such structures has still not been studied extensively in the literature. Therefore, the aim of this study was to evaluate the use of LLLT, 670 nm, at three different doses on the epiphyseal growth of the right tibia of rats. Twenty-one Wistar rats, aged four weeks, were subjected to the application of LLLT, with dosage according to the group (G4: were submitted to the application of 4 J/cm2; G8: were submitted to the application of 8 J/cm2; G16: were submitted to the application of 16 J/cm2). After completion of protocol they were kept until they were 14 weeks of age and then submitted to a radiological examination (evaluation of limb length) and euthanised. The histological analysis of the growth plates (total thickness and hypertrophic and proliferative zones) was then performed. Comparisons were made with the untreated left tibia. No differences were observed in any of the reviews (radiological and histological), when comparing the right sides (treated) to the left (untreated). It was concluded that the treatment with LLLT within the parameters used caused changes neither in areas of the epiphyseal cartilage nor in the final length of limbs.

BALB/c mice are normally more resistant than C57BL/6 (B6) mice to infection with Eimeria vermiformis, but these phenotypes can be reversed by oral or parenteral vaccination with a crude antigen prepared from the parasite. Treatment of mice with antibodies specific for CD4+ or CD8+ T cells showed that the increased susceptibility of vaccinated BALB/c mice was associated with the presence of CD4+ T cells. This finding was confirmed when the recipients of CD4+ T cells selected from the mesenteric lymph nodes (MLN) of vaccinated BALB/c mice produced more oocysts after challenge than the recipients of a similar population of cells from sham-vaccinated mice. The residual population of cells (presumably enriched for CD8+ T cells, 'CD8+'), on the other hand, conferred some protection and, in B6 mice, the findings were reversed. Thus, vaccination induced suppressive or protective CD4+ cells and protective or suppressive 'CD8+' cells, depending upon the normal resistance/susceptibility phenotype of the host. Examinations of the isotypes (IgG1, IgG2a) of specific serum antibodies, and of the levels of IFN-gamma and IL-5 cytokines released by MLN cells stimulated ex vivo, did not allow any further characterization of the mechanisms involved.

The effect of infection and subsequent challenge with Eimeria maxima on the populations of lymphocytes in the small intestine of Light Sussex chickens was assessed by immunohistochemistry. T cells were characterized for CD3, CD4, CD8, TCR1 (gamma delta heterodimer) or TCR2 (alpha beta 1 heterodimer) markers, and B cells for the expression of IgM, IgA and IgG. After a primary inoculum there were, in both the epithelium and the lamina propria, two distinct increases in the numbers of T lymphocytes. The first peaked on days 3-5 and the second, greater influx, on day 11 after infection. CD4+ and CD8+ cells were represented in both peaks but, whereas CD4+ cells were found almost exclusively in the lamina propria, CD8+ cells were present in both sites. The area staining positive for CD8+ cells was somewhat greater than the value obtained for CD4+ cells. In the epithelium there was an early, small increase in TCR1(+)-staining, followed by a larger rise to the second peak, at which time there was also an increase in the lamina propria. Staining for TCR2+ cells followed the same pattern with a reversed distribution between epithelium and lamina propria. Changes after challenge were minimal and confined to the epithelium. The most notable changes in the expression of immunoglobulins were, in the lamina propria, a biphasic increase in the amount of IgM(+)-staining in the course of primary infection (corresponding approximately to that of the T cells), and in IgA+ cells shortly after challenge.

Infection of chickens with Eimeria maxima induces the production of parasite-specific antisera which can be used passively to protect naive chickens against infection. Globulin fractions of these antisera can also be used passively to protect chickens. Similarly, intramuscular injection of soybean lectin affinity purified gametocyte antigens of E. maxima in Freund's Complete Adjuvant induces production of antibodies which are maternally transferred and thereby protect hatchlings against E. maxima. ELISA analyses of serum pools having varying protective capacities revealed good correlations between passive protection and levels of anti-unsporulated oocyst, anti-sporulated oocyst, anti-merozoite and anti-gametocyte antibodies. Western blotting demonstrated that the sera mainly recognized a number of high molecular weight antigens in all developmental stages and that the intensity of the reactions reflected the degree of protection induced by the sera. Sera from birds immunized with gametocyte antigens also recognized high molecular weight antigens from all the developmental stages, with banding patterns remarkably similar to those observed for sera from infected birds. Taken together, these results indicate that antibodies can protect against infection with E. maxima and these antibodies may recognize and act against asexual and/or sexual stages of the parasite.

Cellular and cytokine responses to infection with Eimeria vermiformis were compared in BALB/c (resistant) and C57BL/6 (B6-susceptible) inbred mice. Cellular responses in the mesenteric lymph node (MLN) occurred sooner after primary infection in the resistant BALB/c strain. In contrast, proliferative responses occurred earlier after challenge in B6 mice. Resting levels of CD4 + ve and CD8 + ve T-lymphocytes in the MLN differed between the two strains but the relative numbers of each subset remained relatively constant throughout primary infection. MLN cells taken at intervals after infection were assayed for release of the cytokines IFN-gamma, IL-5 and IL-10 after culture in vitro with the mitogen Concanavalin A (Con-A) or with parasite antigen. With either stimulus cells from resistant BALB/c mice released IFN-gamma and IL-5 earlier after infection than did B6 cells. The strains had a comparable absolute ability to produce IFN-gamma but BALB/c cells released more IL-5 than did B6, levels declining, rather than increasing, during primary infection in the latter. Only cells from BALB/c mice released IL-10 during infection. Cells taken after a secondary infection released relatively little cytokine after pulsing in vitro. These data suggest that the difference in response phenotype between the two strains when infected with E. vermiformis reflect a kinetic, rather than a qualitative, difference in ability to mount protective T-helper (Th) cell subset responses. No evidence was found for a Th2-mediated interference with ability to release IFN-gamma, the cytokine most closely associated with protective immunity.

The effect of treatment with a monoclonal antibody (MoAb) capable of neutralising interferon-gamma (IFN-gamma) on the course of coccidial infections in mice (C57BL/6 and NIH infected with Eimeria vermiformis or E. pragensis, and BALB/c infected with E. pragensis) was examined. The results differed with the species of parasite, the strain of mouse, the measure of infection and whether the infection was a primary or secondary one. The replication of E. vermiformis in primary infections was enhanced in both C57BL/6 and NIH mice, but less MoAb was required in NIH than in C57BL/6 to produce similar effects. In neither strain did treatment prevent priming or interfere with the complete immunity to challenge normally induced by moderate infection with E. vermiformis. The replication of E. pragensis in primary infections was not affected in any of the strains of mouse but the clinical effects were exacerbated. Priming with E. pragensis was unaffected by treatment but the partial immunity to challenge, normally induced by infection with this species, was reduced when MoAb was given 2 h before challenge. This reduction was evident as an increased faecal output of oocysts and loss of body weight. These results confirm the role of IFN-gamma in resistance to coccidiosis and further emphasise the complexity of the immune response in this disease.

In the development of a normal strain, WIS, of Eimeria tenella there are three generations of schizogony whereas in an attenuated line, WIS-F-96, derived from WIS, the second and third are absent. Chickens immunized by infection with WIS-F-96, however, were highly resistant to oral challenge with sporulated oocysts of WIS, and histological studies indicated that the immune response was directed against the sporozoites from that challenge inoculum. When challenge of the WIS-F-96-primed chickens consisted of second generation merozoites of WIS (inoculated intracaecally), immunity was less pronounced and the histological data indicated that the merozoites proceeded to develop normally in these birds. These indications of immunological diversity between the merozoites of the first and second generations of schizogony of E. tenella WIS correlated with the results of preliminary studies of the antigenic composition of these developmental stages.

The necessity for co-operation between lymphocytes and myeloid-derived inflammatory cells in the mediation of anti-coccidial immunity was investigated using mice infected with Eimeria vermiformis. Reciprocal exchange of immune lymphocytes between H-2 compatible strains of contrasting susceptibility to infection (resistant BALB/B and susceptible C57BL/10) resulted in successful transfer of immunity in both homologous and heterologous exchanges. Recipients of immune cells, whatever their original response phenotype, expressed a high degree of immunity to infection, indicating that the differential susceptibility of the strains is a property of their lymphoid cells and is not attributable to their capacity to mount inflammatory responses. This conclusion was confirmed by the successful adoptive transfer of immunity into NIH mice previously exposed to 600 rad X-irradiation; at this level of irradiation inflammatory responsiveness is severely depressed. Additional confirmation that strain-response phenotype is lymphocyte dependent and that immune lymphocytes can mediate their effects against E. vermiformis without the intervention of inflammatory cells was obtained from studies on the mucosal mast cell response to infection. No correlation existed between the development of intestinal mastocytosis, an index of T-cell-mediated inflammatory responsiveness, and the expression of resistance to E. vermiformis in BALB/c (resistant), C57BL/10 (susceptible) and NIH (susceptible) mice.

Peripheral blood lymphocytes of chickens and thoracic duct lymphocytes and mesenteric lymph node cells of rats, were labelled with 125I-deoxyuridine and injected intravenously into chickens or rats respectively. Sixteen to 18 h later the intestines of coccidia infected animals contained more radioactivity than those of uninfected controls. This result was obtained with cell suspensions from both infected and normal donors indicating that, as with nematode infected rodents, the increased homing of the cells to parasitised gut was not antigen specific. In chickens the stimulus which causes the increased homing of cells to the intestine was induced within hours of parasite inoculation. This reflects the rapid response of this host, previously described with other parameters, and which may be characteristic of birds.

The development of a reliable model for the adoptive transfer of immunity to coccidiosis (infection with Eimeria vermiformis in NIH mice) is described. More than 10(8) of a mixture of spleen and mesenteric lymph node (MLN) cells, given either intravenously or intraperitoneally, were required to transfer a significant degree of protection. Dividing cells, present in the donors at 10 or 14 days after priming, but not at 5 or 19 days, were shown to be the effectors. When examined separately, MLN cells were found to be superior to spleen cells, and the injection of as few as 5 x 10(7) was capable of substantially reducing the oocyst output from a challenge inoculum. The recipients of cells from primed mice had earlier, and sometimes higher, titres of specific antibodies in the serum but, overall, there was no correlation between these titres and protection. Further characterization of the cells responsible for adoptively transferring immunity to this infection should now be possible.

The systemic secretion of rat mucosal mast cell protease (RMCPII), a major product of rat mucosal mast cells (MMC), was examined during primary infections with the protozoan parasite, Eimeria nieschulzi in CFH/B, athymic (rnu/rnu) and euthymic (rnu/+) rats. Release of RMCPII into the blood stream (2.9 micrograms/ml of serum) of normal rats occurred within 1 day after infection. This response developed 3-6 hours after inoculation with oocysts, was dose-dependent, and was found in both naive and immune rats. Maximal release of RMCPII (4.5 micrograms/ml of serum) in naive rats occurs 9 days after primary infection, whereas the numbers of MMC and concentrations of mucosal RMCPII were maximal 14 days after infection, by which time the systemic RMCPII response had begun to decline. The numbers of MMC and concentrations of mucosal RMCPII in uninfected nude rats were similar to those in the heterozygous (rnu/+) litter-mates. After infection, the numbers of MMC and concentrations of mucosal RMCPII increased in the heterozygotes but not in nude rats. Similarly, RMCPII was detected systemically only in the heterozygotes.

Suspensions of cells prepared from the caecal tonsils and spleen, and the peripheral blood lymphocytes of chickens immune to Eimeria maxima, were tested for their ability to transfer resistance to syngeneic recipients. The intravenous injection of approximately 6 x 10(8) spleen cells or peripheral blood lymphocytes caused a significant reduction of oocyst production by the challenged recipients, in comparison with controls which were uninjected or given cells from birds susceptible to E. maxima. Peripheral blood lymphocytes appeared to be most effective when obtained 10-15 days after a primary, or 3-10 days after a secondary inoculation of oocysts. The peripheral blood lymphocytes which participate in the early response to challenge of immune birds were not found to be protective. When given intraperitoneally, greater numbers of spleen cells were required to reduce oocyst production, and small numbers of caecal tonsil cells were ineffective. The ability of the various cell suspensions to transfer antibody and cell-mediated responses was monitored with 'marker' antigens. There was some indication that both types of response were involved in protection.

The antibody responses of rats to infection with the intestinal intracellular protozoan parasite Eimeria nieschulzi were examined by a sensitive radio-immunoassay with a soluble preparation of sporulated oocysts as antigen. Specific antibodies of the IgM, IgG1, IgG2a and IgG2b isotypes were found in the blood circulation and IgA antibodies were detected in the bile and in intestinal washings. The IgM response was rapid, its peak was relatively brief and it was not recalled by the reinoculation of oocysts. There were some differences between the responses in the different subclasses of IgG but they all reached a peak between 20-30 days after the initiation of the primary infection and there was an anamnestic response to a challenge inoculation of oocysts. IgA antibodies to E. nieschulzi antigen in the bile and in intestinal washings increased and decreased after both primary and secondary inocula. Antibodies of all isotypes tested were virtually absent in the blood circulation of infected athymic rats. These findings are discussed with reference to antibody responses to other parasitic infections and to the role of antibodies in immunity to coccidiosis.

The effects of three immunosuppressive treatments--whole body irradiation and injections of cortisone acetate or cyclophosphamide, on the course of primary infections with Eimeria vermiformis were investigated in 'resistant' BALB/c and 'susceptible' C57BL/6 mice. Immunosuppression (and the nude athymic mutation in BALB/c mice) resulted in increased reproduction of the parasite in both strains of mice, indicating some immunological control of primary infections. The effect was, however, very much more marked in the BALB/c mice, resulting in an alteration in the relative susceptibilities of the two strains. The findings are discussed and it is suggested that the basis for the differences observed in the course of infection in normal BALB/c and C57BL/6 mice lies in their immune responses to this parasite.

The enzyme-linked immunosorbent assay (ELISA) has been used to study the serum IgM and IgG response and the bile IgA and IgM response of chickens to a primary, secondary and tertiary inoculation of Eimeria tenella. In the serum there was a rapid and transient IgM response to the primary infection; second and third inoculations of oocysts had comparatively little effect on the concentrations of this antibody isotype. This differed from the specific IgG response which was later and of similar magnitude after each inoculum. In the bile, specific IgA reached its highest concentrations 9-10 days after the primary inoculation and then declined rapidly. The second and third inoculations each induced low concentrations of this isotype. The specific biliary IgM response to the primary inoculation was similar in profile to that of the IgA, but IgM was detected only on day 14-15 after the second and not at all after the third inoculation. The findings are discussed and are compared with the results obtained using other host species, principally the rat, and with other gut organisms. The relevance of the antibody response in resistance to eimerian infections is also discussed.

The course of each of three successive infections with Eimeria nieschulzi in nude (athymic) rats was the same as the primary infection in nu/+ animals, with the production of more oocysts. This indicates that resistance to reinfection with this parasite is mediated by T lymphocytes but that these cells do not control the duration of the life cycle, since oocyst production was not prolonged in the nu/nu rats. After the three infections with E. nieschulzi, the rats were exposed twice to the intestinal nematode Nippostrongylus brasiliensis, and the nu/nu were completely susceptible even to the second infection. Egg production by both infections in the nu/nu animals was similar and continued at a high plateau level for 28 days before falling to a low level. It appears that the strain of N. brasiliensis used in this study is unable to sustain high egg production for more than 4 weeks in T cell deficient rats.

The ELISA test was used for the detection of antibodies to coccidia in the serum and/or egg yolk of chickens infected with Eimeria acervulina, E. maxima or E. tenella and in the serum of rats infected with E. nieschulzi. Antigens prepared from different developmental stages of the parasite were tested and the cross-reaction between different species of Eimeria were examined. The variability in cross-reactivity of different species and the advantages and possible applications of the test are discussed.