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Bacillus thuringiensis (Bt) is a rod-shaped, Gram-positive soil bacterium that belongs to the phylum Firmicutes and the genus Bacillus. It is a spore-forming bacterium. During sporulation, it produces a wide range of crystalline proteins that are toxic to different orders of insects. Sporulation, structure assembly, and germination are essential stages in the cell cycle of B. thuringiensis. The majority of studies on these issues have focused on the model organism Bacillus subtilis, followed by Bacillus cereus and Bacillus anthracis. The machinery for sporulation and germination extrapolated to B. thuringiensis. However, in the light of recent findings concerning the role of the sporulation proteins (SPoVS), the germination receptors (Gr), and the cortical enzymes in Bt, the theory strengthened that conservation in sporulation, structure assembly, and germination programs drive the survival and success of B. thuringiensis in the environment and the insect host. In the present minireview, the latter pinpointed and reviewed.

Host immunity to Mycobacterium leprae encompasses a spectrum of mechanisms that range from cellular immunity-driven protection to damage associated with humoral immunity as in type-2 leprosy reactions. Although type I interferons (IFNs) participate in eliminating intracellular pathogens, their contribution to the production of antibodies and CD3+ FOXP3+ regulatory T cells (Tregs) in BCG vaccine-mediated protection in leprosy is unknown. BCGphipps (BCGph) priming followed by intramuscular hIFN-α 2b boost significantly reduced lesion size and Mycobacterium lepraemurium growth in the skin. T follicular regulatory cells (TFR), a subset of Tregs induced by immunization or infection, reside in the germinal centers (GCs) and modulate antibody production. We found impaired Treg induction and improved GCs in draining lymph nodes of BCGph primed and hIFN-α 2b boosted mice. Moreover, these mice elicited significant amounts of IL-4 and IL-10 in serum. Thus, our results support the adjuvant properties of hIFN-α 2b in the context of BCGph priming to enhance protective immunity against skin leprosy.

As a self-degradative and recycling program, autophagy plays an essential role in homeostasis and life. The connection between autophagy and the status of the adipose tissue (white or beige/brown) links to metabolic diseases such as obesity, type two diabetes mellitus (T2DM). Moreover, autophagy and the renin-angiotensin physiological system play a pivotal role in metabolic syndrome, a disease that can disrupt homeostasis in different organs, including adipose tissue. The crosstalk in adipose tissue maintains low inflammation, brown adipocytes, and autophagic machinery under control. The JAK-STAT signalization pathway and the paracrine action of hormones, adipokines, and cytokines play a role in maintaining the status of low inflammation, brown adipocytes, and autophagic machinery to harness the utmost for obesity immunotherapy.

Leprosy is a still a serious human health problema in developed countries. Environmental and genetic factors are playing a key role in the chronic course of the disease, resistance versus susceptibility. The multidrug treatment is not effective for all infected individuals; “cured” individuals mostly show relapses of neurological disordes and potential as the same as not cured can present physical and deformed constrainst. The unsolved puzzle in leprosy is that clinic spectrum depends of the host immune response.and thus, the outcome of the immune response. In the present review we intended to describe some aspects of the immunotherapy, based on type I IFNs and M. bovis BCG vaccine as a strategy such as sword to target germinal centers, either for the generation or for the enhancement and thus, throughout key signals delivered by folicular CD4+ T cells, and controlled by folicular regulatory CD4+ T cells, B cell differentiation into plasmacytoid cells be highly promoted the induction of protective high affinity neutralyzing antibodies to unlock humoral immunity, protective toward M. leprae infected individuals.

Entamoeba histolytica is a protozoan parasite that causes amoebiasis in humans; as the infection occurs mainly in the intestinal epithelium, the secretory immune response of the host could have an influence on the outcome. Secretory IgA antibodies against E. histolytica have been detected in asymptomatic and symptomatic patients, but little is known about their protective role. E. histolytica cysteine proteases seem to be involved in the pathogenesis of amoebiasis; therefore, it is important to evaluate the human IgA response against these proteases and its effect on their enzymatic activity. When human saliva samples with and without antibodies against E. histolytica were tested by Western blot against one purified 70 kDa amoebic cysteine protease, 84% of anti-amoeba-positive samples recognized it. The secretory IgA purified from a pool of anti-protease-positive samples had a strong in vitro inhibitory effect on the E. histolytica proteolytic activity. These results suggest that this effect, if it occurs in vivo, could be an important protective factor against this parasite.

Heterologous prime-boost regimens are a valuable strategy to improve the generation of effector-memory T cell responses against intracellular pathogens. In this study we show that newborn mice vaccinated with bacillus Calmette-Guérin (BCG) and boosted with heparin-binding haemagglutinin (HBHA) had enhanced protective immunity against intranasal or aerosol Mycobacterium tuberculosis challenge over non-boosted mice, as evidenced by a considerable reduction of mycobacterial load in spleen and lung. The route of HBHA delivery had a differential impact on cytokine and antibody production in BCG-primed mice. The prime-boost regimen induced not only HBHA-specific IFN-gamma, but also other cytokines, such as IL-12 and TGF-beta, which may be associated with the generation of lung Th1 effector-memory lymphocytes, responsible for the enhanced protection against M. tuberculosis challenge.

Heparin-binding haemagglutinin (HBHA) is a 28-kDa mycobacterial adhesin, composed of three functional domains. Previous work has shown that the C-terminal methylated domain is important for adherence, and it is involved in protective T cell immunity in mouse models. However, the role of the coiled-coil N-terminal domain of HBHA in its overall immunogenic capacity remains elusive. Herein, a comparison of the antibody and cellular immune responses after subcutaneous and intranasal immunization of mice with HBHA (native and recombinant) revealed that the methylation pattern is important but not essential for this property. Subcutaneous immunization of mice with a truncated protein, rHBHADeltaC, which lacks the C-terminal methylated domain, was sufficient to trigger humoral and cellular immune responses to HBHA in mice. Altogether we provide evidence that the coiled-coil N-terminal domain is required for HBHA immunogenicity in vivo.