ABSTRACT
The interaction of a pathogen with its host cell takes place at different levels, including the bioenergetics adaptation of both the pathogen and the host cell in the course of an infection. In this regard, Mycobacterium tuberculosis infection of macrophages induces mitochondrial membrane potential (Δψm) changes and cytochrome c release, depending on the bacteria strain's virulence, and the mitochondrial dynamics is modified by pathogens, such as Listeria monocytogenes. Here, we investigated whether two M. tuberculosis virulence factors are able to induce distinguishable bioenergetics traits in human monocyte-derived macrophages (MDMs). Results showed that Rv1411c (LprG, p27) induced mitochondrial fission, lowered the cell respiratory rate and modified the kinetics of mitochondrial Ca2+ uptake in response to agonist stimulation. In contrast, Rv1818c (PE_PGRS33) induced mitochondrial fusion, but failed to induce any appreciable effect on cell respiratory rate or mitochondrial Ca2+ uptake. Overall, these results suggest that two different virulence factors from the same pathogen (M. tuberculosis) induce differential effects on mitochondrial dynamics, cell respiration and mitochondrial Ca2+ uptake in MDMs. The timing of differential mitochondrial activity could ultimately determine the outcome of host-pathogen interactions.
Subject(s)
Host-Pathogen Interactions/physiology , Macrophages/microbiology , Mitochondrial Dynamics/physiology , Mycobacterium tuberculosis/pathogenicity , Virulence Factors/metabolism , Bacterial Proteins/metabolism , Humans , Macrophages/metabolism , Tuberculosis/metabolism , Tuberculosis/microbiology , Virulence/physiologyABSTRACT
A wide array of microorganisms colonizes distinctive anatomical regions of animals, being the intestine the one that harbors the most abundant and complex microbiota. Phylogenetic analyses indicate that it is composed mainly of bacteria, and that Bacterioidetes and Firmicutes are the most represented phyla (>90% of the total eubacteria) in mice and humans. Intestinal microbiota plays an important role in host physiology, contributing to digestion, epithelial cells metabolism, stimulation of intestinal immune responses, and protection against intestinal pathogens. Changes in its composition may affect intestinal homeostasis, a condition known as dysbiosis, which may lead to non-specific inflammation and disease. The aim of this work was to analyze the effect that a bacteria-specific systemic immune response would have on the intestinal re-colonization by that particular bacterium. Bacteria were isolated and identified from the feces of Balb/c mice, bacterial cell-free extracts were used to immunize the same mice from which bacteria came from. Concurrently with immunization, mice were subjected to a previously described antibiotic-based protocol to eliminate most of their intestinal bacteria. Serum IgG and feces IgA, specific for the immunizing bacteria were determined. After antibiotic treatment was suspended, specific bacteria were orally administered, in an attempt to specifically re-colonize the intestine. Results showed that parenteral immunization with gut-derived bacteria elicited the production of both anti-bacterial IgG and IgA, and that immunization reduces bacteria specific recolonization of the gut. These findings support the idea that the systemic immune response may, at least in part, determine the bacterial composition of the gut.
Subject(s)
Escherichia coli/immunology , Gastrointestinal Microbiome/immunology , Immunization/methods , Intestines/immunology , Staphylococcus aureus/immunology , Animals , Antibodies, Bacterial/immunology , Bacterial Infections/immunology , Bacterial Infections/microbiology , Dysbiosis/immunology , Dysbiosis/physiopathology , Escherichia coli/physiology , Feces/microbiology , Gastrointestinal Microbiome/physiology , Immunoglobulin A/immunology , Immunoglobulin G/immunology , Intestines/microbiology , Male , Mice, Inbred BALB C , Staphylococcus aureus/physiologyABSTRACT
Se presenta el caso de anafilaxia a lidocaína en una paciente sometida a analgesia epidural para trabajo de parto, la cual desarrolló inmediatamente después de la aplicación de una dosis de prueba de lidocaína (PISA). La anafilaxia al anestésico local se comprobó mediante la determinación del factor inhibidor de leucocitos y del porcentaje de degranulación de basófilos
Subject(s)
Humans , Female , Pregnancy , Labor, Obstetric/drug effects , Histamine H1 Antagonists/administration & dosage , Histamine H1 Antagonists/therapeutic use , Anaphylaxis/surgery , Anaphylaxis/complications , Anesthesia, Epidural/adverse effects , Lidocaine/administration & dosage , Lidocaine/adverse effects , Hydrocortisone/administration & dosage , Ephedrine/administration & dosageABSTRACT
Herpes zóster sistémico (Hz) es una enfermedad viral grave, común en pacientes que reciben tratamiento para linfoma o leucemia. También lo padecen pacientes tratados con medicamentos inmunodepresores, así como los individuos inmunodeficientes. En todos esos pacientes la enfermedad no mejora con tratamiento convencional. Este trabajo presenta los resultados del tratamiento con extracto dializable de leucocitos (factor de transferencia), aplicado a ocho pacientes con Hz. Antes del tratamiento los pacientes presentaron disminución de inmunidad mediada por células (por ejemplo, linfocitos sanguíneos T reducidos, prueba cutánea y FIL negativa a tres o cuatro antígenos comunes y aumento de rosetas EAC o células "B"). Los ocho pacientes tratados mostraron, con dos unidades de factor de transferencia (1 unidad = extracto de leucocitos de 6.8 x 10**8), una mejoría clínica notable y, con seis unidades más, los síntomas desaparecieron por completo. Despúes del tratamiento, las pruebas inmunitarias de los pacientes mejoraron o volvieron a la normalidad. Después del estudio, los pacientes se vigilaron durante un año sin presentarse alguna recidiva