Pesticide toxicity, both acute and chronic, is a global public health concern. Pesticides are involved in abnormal inflammatory responses by interfering with the normal physiology and metabolic ...status of cells. In this regard, inflammatory indices aggregate index of systemic inflammation (AISI), monocyte-to-high-density lipoprotein ratio, monocyte-to-lymphocyte ratio (MLR), neutrophil-to-lymphocyte platelet ratio (NLPR), neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, systemic immune inflammation index, and systemic inflammation response index (SIRI) have been used as predictive markers of inflammatory status in several diseases and also in acute poisoning events. This study aimed to determine systemic inflammation indices and their relationship with pesticide exposure from urban sprayers in 302 individuals categorized into three groups (reference group and moderate and high exposure groups). The data suggest that the AISI, MLR, NLPR, and SIRI indices were significantly higher in the exposed groups compared with the reference group. In conclusion, this study proposes that inflammation indices warrant further attention in order to assess their value as early biomarkers of acute and chronic pesticide intoxication.
Aim
Ankylosing spondylitis (AS) pathogenesis has focused on the adaptive immune response; however, innate immune responses may also play a role in the inflammatory response of AS. Dysregulated ...neutrophil activation can induce tissue damage and contribute to the pathogenesis of immune‐related diseases. Hence, the aim of this study was to assess the effect of immune complexes formed with the p30 of Salmonella typhimurium and anti‐p30 antibodies present in the sera of AS patients and controls in inducing the release of neutrophil extracellular traps (NETs) and the secretion of pro‐inflammatory cytokines.
Methods
We collected polymorphonuclear leukocytes (PMNs) from healthy donors. The PMNs isolated were stimulated with p30 alone or in immunocomplexes formed with antibodies presents in sera of AS patients or control subjects. Then, the NETs were analyzed by fluorescence microscopy. Concentrations of interleukin (IL)‐6, tumor necrosis factor (TNF)‐α, IL‐1β, IL‐8 and IL‐10, were determined using the Cytometric Bead Array kit.
Results
Significant difference was observed in the release of NETs between the neutrophils stimulated with p30 + AS (70.52 ± 16.24) those unstimulated neutrophils (9.94 ± 12.12; P = .0095), stimulated with phorbol 12‐myristate 13‐acetate (39.78 ± 14.50; P = .0190), stimulated with control serum (CS) (10.85 ± 5.33; P = .0082) and serum of AS patient (10.28 ± 6.15; P = .0087). The stimulation of neutrophils with p30 alone induced a relatively low production of IL‐6 (64.5 pg/mL), IL‐8 (2658.3 pg/mL), IL‐1β (31.11 pg/mL), and TNF‐α (3.8 pg/mL), compared to p30 + AS and p30 + CS groups.
Conclusion
Our results show that neutrophils release NETs and pro‐inflammatory cytokines in response to p30 in immunocomplexes. These findings could improve our understanding of the role of innate immunity in the initiation and/or maintenance of inflammatory responses, and in the progression of AS.
The epidemiological association between exposure to particulate matter (PM
) and various respiratory and cardiovascular problems is well known, but the mechanisms driving these effects remain ...unclear. Neutrophils play an essential role in immune defense against foreign agents and also participate in the development of inflammatory responses. However, the role of these cells in the PM
induced inflammatory response is not yet fully established. Thus, this study aims to evaluate the effect of PM
on the neutrophil-mediated inflammatory response. For this, neutrophils from healthy adult human donors were in vitro exposed to different concentrations of PM
. The cell viability and cytotoxic activity were evaluated by MTT. LDH, propidium iodide and reactive oxygen species (ROS) were quantified by flow cytometry. Interleukin 8 (IL-8) expression, peptidyl arginine deiminase 4 (PAD
), myeloperoxidase (MPO), and neutrophil elastase (NE) expression were measured by RT-PCR. IL-8 was also quantified by ELISA. Fluorescence microscopy was used to evaluate neutrophil extracellular traps (NETs) release. The in vivo inflammatory responses were assessed in BALB/c mice exposed to PM
by histopathology and RT-PCR. The analysis shows that PM
exposure induced a cytotoxic effect on neutrophils, evidenced by necrosis and LDH release at high PM
concentrations. ROS production, IL-8, MPO, NE expression, and NETs release were increased at all PM
concentrations assessed. Neutrophil infiltration in bronchoalveolar lavage fluid (BALF), histopathological changes with inflammatory cell infiltration, and CXCL1 expression were observed in PM
-treated mice. The results suggest that lung inflammation in response to PM
could be mediated by neutrophils activation. In this case, these cells migrate to the lungs and release pro-inflamatory mediators, including ROS, IL-8, and NETs. Thus, contributing to the exacerbation of respiratory pathologies, such as allergies, infectious and obstructive diseases.
Th17 Cells in Autoimmune and Infectious Diseases José Francisco Zambrano-Zaragoza; Enrique Jhonatan Romo-Martínez; Ma. de Jesús Durán-Avelar ...
International Journal of Inflammation,
01/2014, Letnik:
2014, Številka:
2014
Journal Article
Recenzirano
Odprti dostop
The view of CD4 T-cell-mediated immunity as a balance between distinct lineages of Th1 and Th2 cells has changed dramatically. Identification of the IL-17 family of cytokines and of the fact that ...IL-23 mediates the expansion of IL-17-producing T cells uncovered a new subset of Th cells designated Th17 cells, which have emerged as a third independent T-cell subset that may play an essential role in protection against certain extracellular pathogens. Moreover, Th17 cells have been extensively analyzed because of their strong association with inflammatory disorders and autoimmune diseases. Also, they appear to be critical for controlling these disorders. Similar to Th1 and Th2 cells, Th17 cells require specific cytokines and transcription factors for their differentiation. Th17 cells have been characterized as one of the major pathogenic Th cell populations underlying the development of many autoimmune diseases, and they are enhanced and stabilized by IL-23. The characteristics of Th17 cells, cytokines, and their sources, as well as their role in infectious and autoimmune diseases, are discussed in this review.
Aim
Nonalcoholic fatty liver disease (NAFLD) is a complex metabolic condition in which both lifestyle and genetic factors have a pathogenic role. The LEP gene encodes leptin, which regulates ...appetite, body weight, and several metabolic functions. Proopiomelanocortin (POMC), regulates food intake and energy balance. The aim of the study was to determine partial or complete deletions of genes associated with obesity in patients diagnosed with NAFLD.
Material and methods
Blood samples and DNA from 43 individuals diagnosed with NAFLD by ultrasonographic technique (Fibroscan) were obtained. The partial or complete deletions of genes were determined by MLPA (Multiplex Ligation‐dependent Probe Amplification) using the SALSA probemix P220‐B2 Obesity only on 43 individuals. Fifty blood samples from healthy individuals were included.
Results
Eleven out of 43 individuals analyzed by MLPA presented some deletion of the genes analyzed: six were female and five were male. The partial or complete deletion of the LEPR and POMC genes was observed in eight patients (18.6%), SIM1 in six patients (13.9%), GRIK2 and SH2B1 in two patients (4.7%), SEZGL2 in four patients (9.3%), and MCR4 in one patient (2.3%).
Conclusion
Partial deletion was observed in LEPR, POMC, SIM1, GRIK2, SH2B1, SEZGL2, and MCR4 genes in 26% of the cases, and we suggest that these alterations probably has a potential relationship for the development of NAFLD.
Liver cirrhosis (LC) is an inflammatory process associated with impaired functions in adaptive and innate immune responses at both systemic and local levels, also referred as Cirrhosis‐Associated ...Immune Dysfunction. In this study, we evaluated the functionality of neutrophils from ascitic fluid (AF) of patients with hepatic cirrhosis by testing their ability to generate neutrophil extracellular traps (NETs) in vitro. To further determine the activation state of neutrophils, expression of the activation markers CD66b, CD69, and CD80 on these cells was analysed by flow cytometry. The inflammatory environment in AF was assessed by measured concentration of pro‐ and anti‐inflammatory cytokines. Samples were collected from 40 patients with LC, 20 of them with uncomplicated ascites (ASC) and 20 with spontaneous bacterial peritonitis (SBP). Peripheral blood (PB) neutrophils from healthy individuals were used as control (HC). Our results revealed a significant decrease in the release of NETs in neutrophils from the SBP group compared with HC. Low expression of CD69 and CD80 on neutrophils from AF of SBP patients was also observed. Comparisons of inflammatory cytokine levels in AF from the different study groups (SBP and ASC) revealed significant differences. In conclusion, we demonstrate that the development of complications, such as SBP, increases initially the inflammatory status, but chronically results in impaired neutrophil function as demonstrated by the decreased capability of NETs formation. There is also an increase in both pro‐inflammatory and anti‐inflammatory cytokines, thus predisposing for new episodes of SPB and increasing morbidity and mortality in cirrhotic patients.
DNAM-1 (CD226) is an activating receptor expressed in CD8+ T cells, NK cells, and monocytes. It has been reported that two SNPs in the
gene, rs763361 C>T and rs727088 G>A, have been associated with ...different autoimmune diseases; however, the role of DNAM-1 in ankylosing spondylitis has been less studied. For this reason, we focused on the study of these two SNPs in association with ankylosing spondylitis. For this, 34 patients and 70 controls were analyzed using endpoint PCR with allele-specific primers. Our results suggest that rs763361 C>T is involved as a possible protective factor under the CT co-dominant model (OR = 0.34, 95% CI = 0.13-0.88,
= 0.022) and the CT + TT dominant model (OR = 0.39, 95% CI = 0.17-0.90,
= 0.025), while rs727088 G>A did not show an association with the disease in any of the inheritance models. When analyzing the relationships of the haplotypes, we found that the T + A haplotype (OR = 0.31, 95% CI = 0.13-0.73,
= 0.0083) is a protective factor for developing the disease. In conclusion, the CT and CT + TT variants of rs763361 C>T and the T + A haplotype were considered as protective factors for developing ankylosing spondylitis.
Acute hepatopancreatic necrosis disease (AHPND) was first reported in China in 2009 and afterwards in Mexico in 2013. AHPND is caused by Vibrio parahaemolyticus and affects Penaeus monodon and ...Litopenaeus vannamei shrimp cultures. The bacterium contains the pirA‐ and pirB‐like genes in 69‐ to 70‐Kb plasmids, which encode the toxins that produce the disease. The aim of this study was to determine whether pirA‐ and pirB‐like genes existed in bacterial genera distinct from Vibrio before the first cases of AHPND were documented in Mexico. Two bacterial isolates were selected from shrimp farms in Nayarit in 2006 and analysed by nested‐PCR to determine the presence of pirA‐ and pirB‐like genes. The two isolates chosen did indeed show the presence of these genes, and those findings were confirmed by sequencing. Both strains matched to the bacterial species Micrococcus luteus. Results revealed two important situations: (a) the pirA‐ and pirB‐like genes were present in a bacterial species that has not been reported previously (Micrococcus luteus); and (b) pirA‐ and pirB‐like bacterial genes were present in Mexico before the first AHPND outbreak was reported in China.
DNAM-1 (CD226) is an activating receptor expressed in CD8+ T cells, NK cells, and monocytes. It has been reported that two SNPs in the DNAM-1 gene, rs763361 C>T and rs727088 G>A, have been associated ...with different autoimmune diseases; however, the role of DNAM-1 in ankylosing spondylitis has been less studied. For this reason, we focused on the study of these two SNPs in association with ankylosing spondylitis. For this, 34 patients and 70 controls were analyzed using endpoint PCR with allele-specific primers. Our results suggest that rs763361 C>T is involved as a possible protective factor under the CT co-dominant model (OR = 0.34, 95% CI = 0.13–0.88, p = 0.022) and the CT + TT dominant model (OR = 0.39, 95% CI = 0.17–0.90, p = 0.025), while rs727088 G>A did not show an association with the disease in any of the inheritance models. When analyzing the relationships of the haplotypes, we found that the T + A haplotype (OR = 0.31, 95% CI = 0.13–0.73, p = 0.0083) is a protective factor for developing the disease. In conclusion, the CT and CT + TT variants of rs763361 C>T and the T + A haplotype were considered as protective factors for developing ankylosing spondylitis.
Rheumatoid arthritis (RA) is a chronic inflammatory disease whose association with SNPs has led to the identification of biomarkers in different populations. To determine the association of the ...-857C/T SNP of the TNFA gene with RA and clinical parameters, 233 RA patients and 237 healthy controls were included in this study. The -857C/T polymorphism was determined using the TaqMan® system and clinical features were also determined. We found that the -857C/T SNP was in Hardy-Weinberg equilibrium. Our results showed no association of the -857C/T SNP with RA; however, RA patients carrying the TT genotype showed lower anti-CCP levels than other groups. Therefore, the TT genotype could be a risk factor for developing anti-CCP-negative RA. Our results suggest that the T allele of the TNFA -857C/T SNP exerts an influence on anti-CCP levels and could be a candidate marker for anti-CCP-negative RA.
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