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Analysis of annexin 1 expression in rat trachea: Study of the mast cell heterogeneity
... The detection of endogenous ANXA1 on leukocytes was performed as previously described 13 . The slides were incubated with a rabbit anti-ANXA1 primary antibody (1:200 in 1% BSA) (Invitrogen™). ...
... Other studies have reported similar results [14][15][16][17] . The infection caused by M. leprae induces a specific immune response that is directly associated with the clinical form existing in the individual [10][11][12][13][14][15] . Leukocyte recruitment to an inflammatory site is mainly triggered by a strong Th1 response, resulting in granuloma formation, predominantly formed by histiocytes and lymphocytes, in an attempt to eliminate the bacillus 21-28 . ...
... ANXA1 is an important protein modulator of acute inflammatory activity involved in the inhibition of leukocyte extravasation to the site of inflammation 6,7,29 . This molecule has been studied to elucidate the mechanisms that operate in the host during the resolution of the inflammatory process 6,7,13 . In this study, tuberculoid patients had reduced expression of ANXA1 in circulating polymorphonuclear cells when compared to lepromatous patients. ...
INTRODUCTION
In leprosy, immune system mediators that regulate the infectious process act in a complex manner and can lead to several clinical outcomes. To understand the behavior of these mediators we quantified the expression of annexin-A1 (ANXA1) in the peripheral blood and plasma as well as tissue leukocytes in all clinical forms of leprosy and compared with healthy controls.
METHODS
Seventy healthy controls and 70 patients with leprosy, tuberculoid (TT) (n = 13), borderline tuberculoid (BT) (n = 15), borderline borderline (BB) (n = 13), borderline lepromatous (BL) (n = 15), and lepromatous leprosy (LL) (n = 14), were selected. Phenotyping of the lymphocyte cells and the intracellular expression of ANXA1 in leukocytes was performed by immunofluorescence. Plasma protein levels were determined by enzyme-linked immunosorbent assay.
RESULTS
Histiocytes and CD4⁺ and CD8⁺ T cells in the skin of BL and LL patients had higher ANXA1 expression. ANXA1 expression was also high in circulating polymorphonuclear, monocytes, and CD4⁺ and CD8⁺ T cells in the blood of LL patients compared to those of TT, BT, BB, and BL patients, and these levels were similar to those in healthy controls. Plasma ANXA1 levels indicate an increase in paracrine release in patients with LL.
CONCLUSIONS
The data indicate that ANXA1 expression is enhanced in the leukocytes and plasma of patients with LL, and may contribute to the inhibition of leukocyte action, leading to inadequate functioning of the immune system and thus contributing to the spread of M. leprae infection.
... We included 17 patients, all above 18 years, who attended the rheumatology medical clinic at the University of Cuiabá between July 2017 and September 2022. These patients were categorized based on the chikungunya fever diagnostic criteria 10 . Following their initial consultation and diagnosis of CHIKV articular disease, they underwent clinical and laboratory evaluations every three months if symptoms persisted. ...
... The slides were mounted on Citiflour (DAKO, USA) and analyzed by a single analyzer using an AxioScope A1 microscope and the Axiovision software (Carl Zeiss, GR). Immunofluorescence was scored as follows: 0 = no signal; 1 = faintly marked cells; 2 = moderate; 3 = intense; 4 = very intense fluorescence detected 10 . ...
Introduction
Chikungunya chronic joint disease causes debilitating arthralgia, significantly impacting the quality of life of affected individuals.
Methods
In this study, patients underwent clinical follow-ups, joint biopsies, and pre-biopsy and 24 months post-biopsy serum dosage of cytokines.
Results
All participants were female and had pain in 12 joints on average, with 41.17% exhibiting moderate disease activity. Histopathological analysis revealed collagen deposition. Indirect immunofluorescence detected the CHIKV glycoprotein E1 antigen, and an increase in cytokines.
Conclusions
Persistent inflammation and ineffective antiviral immune responses leading to antigen persistence may contribute to chronic CHIKV arthritis.
Keywords:
Chikungunya; Inflammatory; Cytokines
... [8] Annexins are considered the primary mediators of the inflammatory actions of endogenous and exogenous corticosteroids, especially dexamethasone. [11] In situations when the synthesis of annexins is reduced, the therapeutic action of these steroids is decreased, [12,13] and it has been suggested that the failure of corticosteroid therapy in the treatment of phimosis is due to the decreased expression of annexins. [1] Regarding the anti-inflammatory effect of topical corticosteroids, their immunosuppressive action is well known, and this action is attributed to the inhibition of phagocytic activity and leukocyte migration. ...
Introduction:
Histopathological analysis of the foreskin has become more common in the last two decades.
Objectives:
This study aims to analyze the morphology of the foreskin and determine the effects of topical corticosteroid therapy on this tissue.
Materials and methods:
We retrospectively evaluated forty foreskin samples from children aged from 2 years to 15 years with phimosis undergoing circumcision at our institution over a 2-year period. In the foreskin samples, we analyzed the elastic fibers (Verhoeff), epidermal thickness (hematoxylin and eosin), and Annexin 1 and Langerhans cells (LCs) (immunohistochemistry).
Results:
In the present study, 18 (45%) patients made use of topical corticosteroids, and 22 (55%) did not, while 4 (10%) had a history of balanoposthitis as previous complication. Forty patients were divided according to the parameter analyzed: with or without previous complication and with or without previous topical corticotherapy. Annexin 1 expression was significantly higher in group with a history of complications when compared with group without complications (P = 0.024) and lower in the group of those who used corticosteroids when compared with those who did not used corticosteroids (P = 0.364). In the analysis of all samples, the density of mature LCs was significantly higher when compared with immature LCs (P < 0.0001). The density of immature LCs was significantly higher in patients without previous complications when compared with group with complications (P = 0.028).
Conclusions:
These findings contribute to a better understanding of the histopathological aspects of previous complications and of treatment with corticosteroids in children with phimosis.
... Blood smears of patients infected with P. vivax and healthy controls were incubated with 5% albumin bovine in PBS (PBSA) to block nonspecific binding and permeabilized with Teen 20 at 0.4% in PBS, as described before [22]. A cocktail of primary antibodies were used to identify ANXA1 expression and lymphocyte subpopulation. ...
... ANXA1 expression is altered in mast cells in inflammatory diseases and cancer. In the trachea and mesentery of rats, mast cells express more ANXA1 after treatment with dexamethasone, suggesting that glucocorticoids inhibit degranulating mast cells [29,30,35]. Similarly, pretreatment of mice with Ac2-26 (the N-terminal region of ANXA1) increases the number of intact mast cells in the pleural cavity and decreases the release of histamine in a model of ovalbumin-induced allergic inflammation, confirming the protective effect of ANXA1 in their activation [36]. ...
... Blood smears of patients infected with P. vivax and healthy controls were incubated with 5% albumin bovine in PBS (PBSA) to block nonspecific binding and permeabilized with Teen 20 at 0.4% in PBS, as described before [22]. A cocktail of primary antibodies were used to identify ANXA1 expression and lymphocyte subpopulation. ...
Malaria is the most prevalent parasitic disease in the world. In Brazil, the largest number of malaria cases (98%) is within the Legal Amazon region, where Plasmodium vivax is responsible for over 80% of diagnosed cases. The aim of this study was to investigate the annexin-A1 expression in CD4+, CD8+ T cells, regulatory T cells (Treg) and cytokine IL-10 quantification in plasma from patients with malaria caused by P. vivax.
The quantification of the cytokine IL-10 of patients infected with P. vivax and healthy controls were evaluated by enzyme-linked immunosorbent assay (ELISA). The determination of the expression of annexin-A1 in lymphocytes from patients and healthy controls was determined by immunofluorescence staining. All results were correlated with the parasitaemia and the number of previous episodes of malaria.
The cytokine IL-10 plasma levels showed a significant increase in both patients with low (650.4 +/- 59.3 pg/mL) and high (2870 +/- 185.3 pg/mL) parasitaemia compared to the control (326.1 +/- 40.1 pg/mL). In addition, there was an increase of this cytokine in an episode dependent manner (individuals with no previous episodes of malaria - primoinfected: 363.9 +/- 31.1 pg/mL; individuals with prior exposure: 659.9 +/- 49.4 pg/mL). The quantification of annexin-A1 expression indicated a decrease in CD4+ and CD8+ T cells and an increase in Treg in comparison with the control group. When annexin-A1 expression was compared according to the number of previous episodes of malaria, patients who have been exposed more than once to the parasite was found to have higher levels of CD4+ T cells (96.0 +/- 2.5 A.U) compared to primoinfected (50.3 +/- 1.7). However, this endogenous protein had higher levels in CD8+ (108.5 +/- 3.1) and Treg (87.5 +/- 2.5) from patients primoinfected.
This study demonstrates that in the patients infected with P. vivax the release of immunoregulatory molecules can be influenced by the parasitaemia level and the number of previous episodes of malaria. annexin-A1 is expressed differently in lymphocyte sub-populations and may have a role in cell proliferation. Furthermore, annexin-A1 may be contributing to IL-10 release in plasma of patients with vivax malaria.
... This discrepancy can be explained by the high levels of cleaved AnxA1 (33 kDa) observed after intestinal I/R by Western blotting technique. One of the possible posttranslational modifications described for these proteins is phosphorylation, which leads to protein translocation to the membrane and release during the inflammatory process34353637. Future studies will therefore address the secreted levels of AnxA1 after intestinal I/R. ...
Background
Intestinal ischemia/reperfusion (IR) injury is a serious and triggering event in the development of remote organ dysfunction, from which the lung is the main target. This condition is characterized by intense neutrophil recruitment, increased microvascular permeability. Intestinal IR is also responsible for induction of adult respiratory distress syndrome, the most serious and life-threatening form of acute lung injury. The purpose of this study was to investigate the effect of annexin-A1 protein as an endogenous regulator of the organ remote injury induced by intestinal ischemia/reperfusion. Male C57bl/6 mice were subjected to intestinal ischemia, induced by 45 min occlusion of the superior mesenteric artery, followed by reperfusion.
Results
The intestinal ischemia/reperfusion evoked a high intensity lung inflammation as indicated by the number of neutrophils as compared to control group. Treatment with annexin-A1 peptidomimetic Ac2-26, reduced the number of neutrophils in the lung tissue and increased its number in the blood vessels, which suggests a regulatory effect of the peptide Ac2-26 in the neutrophil migration. Moreover, the peptide Ac2-26 treatment was associated with higher levels of plasma IL-10.
Conclusion
Our data suggest that the annexin-A1 peptidomimetic Ac2-26 treatment has a regulatory and protective effect in the intestinal ischemia/reperfusion by attenuation of the leukocyte migration to the lung and induction of the anti-inflammatory cytokine IL-10 release into the plasma. The anti-inflammatory action of annexin-A1 and its peptidomimetic described here may serve as a basis for future therapeutic approach in mitigating inflammatory processes due to intestinal ischemia/reperfusion.
... ANXA1 expression is altered in mast cells in inflammatory diseases and cancer. In the trachea and mesentery of rats, mast cells express more ANXA1 after treatment with dexamethasone, suggesting that glucocorticoids inhibit degranulating mast cells [29,30,35]. Similarly, pretreatment of mice with Ac2-26 (the N-terminal region of ANXA1) increases the number of intact mast cells in the pleural cavity and decreases the release of histamine in a model of ovalbumin-induced allergic inflammation, confirming the protective effect of ANXA1 in their activation [36]. ...
This study evaluated the properties of endogenous nitric oxide synthases (NOS) and annexin-A1 (ANXA1) and determined how they can be exploited in the N-methyl-N-nitro-N-nitrosoguanidine (MNNG)-induced gastric carcinogenesis and myenteric denervation model. Male Wistar rats were treated with MNNG and/or aminoguanidine (AG) for 20 weeks. In another set of experiments, rats with nondenervated and denervated stomachs were treated with MNNG or water for 28 weeks. Fragments of the pyloric region were processed for histopathology, NOS activity, and immunohistochemistry to explore the activity and expression of constitutive (cNOS) and inducible (iNOS) NO synthase and their relationship with annexin-A1 (ANXA1) expression. NO inhibition by AG increased the percentage of animals with adenocarcinomas (~29%) compared with the untreated MNNG group (~4%). Myenteric denervation did not alter NOS activity. cNOS activity was significantly greater in nondernervated and denervated stomachs with or without lesions (P<0.001) than iNOS activity (P<0.01), as confirmed by immunohistochemistry. Further, cNOS activity in normal stomachs and outside the lesion area was considerably higher than inside it (P<0.01). By densitometric analysis of nondenervated and denervated stomachs, ANXA1 expression was modulated in epithelial and inflammatory cells (mast cells and neutrophils), wherein significant alterations were induced by lesion development and myenteric denervation. In conclusion, NO protects against the development of gastric adenocarcinomas. The pattern of ANXA1 expression was not associated with NOS activity or expression, suggesting that NO and ANXA1 act in gastric tumors in disparate pathways.
Introduction:
Cutaneous leishmaniasis is caused by protozoa of the genus Leishmania and transmission occurs through the bite of sandflies. It is an infectious disease, which affects skin and mucosa. The aim was to quantify the macrophages M1 and M2 and the annexin A1 expression in the skin lesions of patients with cutaneous leishmaniasis.
Methods:
Skin biopsies from patients (n = 50) were analyzed and classified according to the lesion type as: exudative cellular reaction, exudative granulomatous reaction, exudative necrotic reaction, exudative necrotic-granulomatous reaction. Using the immunofluorescence technique, macrophages were identified by CD163 marker, differentiated by anti-MHCII and anti-CD206 antibodies, and annexin A1 expression was determined by arbitrary unit (a.u.) densitometry.
Results:
In M1 macrophages, a greater expression of this protein was observed in the exudative cellular reaction type lesions (136.3 ± 2.6 a.u., assuming mean and standard derivation) when compared to the expression in the lesions of exudative granulomatous reaction, exudative necrotic reaction and exudative necrotic-granulomatous reaction patients (108.0 ± 2.3, 121.6 ± 3.2 and 124.7 ± 2.4 a.u., respectively). Regarding M2 macrophages, it was observed that patients with exudative cellular reaction lesion also had a higher expression of this protein (128.8 ± 2.6 a.u.), when compared to the expression in the lesions of exudative granulomatous reaction, exudative necrotic reaction and exudative necrotic-granulomatous reaction patients (105.6 ± 2, 113.9 ± 2.8, 114.3 ± 2.1 a.u., respectively).
Conclusions:
These data suggest that annexin A1 is assisting macrophages in the phagocytosis process of patients with exudative cellular reaction lesion type.
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