Rapid onset of ICAM-1 expression is a marker of effective macrophages activation during infection of Francisella tularensis LVS in vitro

Novosad, Jakub; Holická, Monika; Novosadová, Martina; Krejsek, Jan; Krčmová, Irena

doi:10.1007/s12223-011-0028-y

Cited by 7 publications

(5 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast, ICAM-1 expression on endothelial cells was not changed 4 days after stroke, possibly because responsive endothelial AM expression peaks earlier ( Jander et al, 1995 ; Yilmaz and Granger, 2008 ). Leukocytic ICAM-1 expression occurs primarily on monocytes/macrophages and enhances endothelial transmigration by homotypic leukocyte–leukocyte interactions ( Goebeler et al, 1993 ; Meisel et al, 1998 ; Ruetten et al, 1999 ; Steidl et al, 2000 ; Novosad et al, 2011 ). ICAM-1 expression on antigen presenting cells may further act as an important costimulatory signal for T cell activation at the site of inflammation ( Goebeler et al, 1993 ; Real et al, 2004 ).…”

Section: Discussionmentioning

confidence: 99%

Arterial Hypertension Aggravates Innate Immune Responses after Experimental Stroke

Möller

Pösel

Kranz

et al. 2015

Front. Cell. Neurosci.

View full text Add to dashboard Cite

Arterial hypertension is not only the leading risk factor for stroke, but also attributes to impaired recovery and poor outcome. The latter could be explained by hypertensive vascular remodeling that aggravates perfusion deficits and blood–brain barrier disruption. However, besides vascular changes, one could hypothesize that activation of the immune system due to pre-existing hypertension may negatively influence post-stroke inflammation and thus stroke outcome. To test this hypothesis, male adult spontaneously hypertensive rats (SHRs) and normotensive Wistar Kyoto rats (WKYs) were subjected to photothrombotic stroke. One and 3 days after stroke, infarct volume and functional deficits were evaluated by magnetic resonance imaging and behavioral tests. Expression levels of adhesion molecules and chemokines along with the post-stroke inflammatory response were analyzed by flow cytometry, quantitative real-time PCR and immunohistochemistry in rat brains 4 days after stroke. Although comparable at day 1, lesion volumes were significantly larger in SHR at day 3. The infarct volume showed a strong correlation with the amount of CD45 highly positive leukocytes present in the ischemic hemispheres. Functional deficits were comparable between SHR and WKY. Brain endothelial expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and P-selectin (CD62P) was neither increased by hypertension nor by stroke. However, in SHR, brain infiltrating myeloid leukocytes showed significantly higher surface expression of ICAM-1 which may augment leukocyte transmigration by leukocyte–leukocyte interactions. The expression of chemokines that primarily attract monocytes and granulocytes was significantly increased by stroke and, furthermore, by hypertension. Accordingly, ischemic hemispheres of SHR contain considerably higher numbers of monocytes, macrophages and granulocytes. Exacerbated brain inflammation in SHR may finally be responsible for larger infarct volumes. These findings provide an immunological explanation for the epidemiological observation that existing hypertension negatively affects stroke outcome and mortality.

show abstract

Section: Discussionmentioning

confidence: 99%

Arterial Hypertension Aggravates Innate Immune Responses after Experimental Stroke

Möller

Pösel

Kranz

et al. 2015

Front. Cell. Neurosci.

View full text Add to dashboard Cite

show abstract

“…Monocyte-macrophage differentiation is associated with decreased expression of monocyte surface markers and increased expression of macrophage markers (40). The classic macrophage surface markers such as CD16 (41), CD68 (42), HLA-DRA (43), ICAM1 (44) and CD38 (45) were considerably increased over the 24-hour time course and the monocyte marker CD14 (46) had reduced expression in differentiated U937 cells (Fig. 1B).…”

Section: Resultsmentioning

confidence: 97%

Macrophage differentiation is marked by increased abundance of the mRNA 3’ end processing machinery, altered poly(A) site usage, and sensitivity to the level of CstF64

Mukherjee

Graber

Moore

2022

Preprint

View full text Add to dashboard Cite

Alternative polyadenylation (APA) results in mRNA isoforms that vary in the amount of coding sequence or 3′ UTR regulatory elements. APA is important for response to external signals and differentiation in several cell types, but its role in differentiation of monocytes to macrophages has not been investigated. Macrophages are key effectors of the innate immune system that help control infection and promote tissue-repair. However, overactivity of macrophages contributes to pathogenesis of many diseases. In this study, we show that macrophage differentiation is characterized by shortening and lengthening of mRNAs in relevant cellular pathways. The cleavage/polyadenylation (C/P) proteins increase during differentiation, suggesting a possible mechanism for APA changes. This was surprising since higher C/P protein levels correlate with higher proliferation rates in other systems, but monocytes stop dividing after induction of differentiation. Depletion of CstF64, a C/P protein and known APA regulator, delayedmacrophage marker expression, cell cycle exit, attachment, and acquisition of structural complexity, and impeded shortening of mRNAs with functions relevant to macrophage biology. Conversely, CstF64 overexpression increased use of promoter-proximal poly(A) sites and caused the appearance of differentiated phenotypes in the absence of induction. Our findings indicate that regulation of polyadenylation plays an important role in macrophage differentiation.

show abstract

“…Macrophages are more effective in killubg the intracellular pathogen when they are co-stimulated by the IFN-γ (ref. 37,38 ). Here, we used IFN-γ as a marker of the progress of the infection.…”

Section: Resultsmentioning

confidence: 99%

Organs of BALB/c mice can be injured in course of tularemia

Pavliš¹,

Kusakova²,

Novotný³

et al. 2014

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

View full text Add to dashboard Cite

Background. Francisella tularensis is a biological agent exploitable for bioterrorism and biological warfare purposes due to serious pathogenic progression and easy dissemination. Despite intensive research in the past, some adverse consequences remain unclear. One consequence of this pathogen is oxidative stress. Aims. The aim of this study was to undertake ex vivo assays for monitoring the disease in mice and increase our knowledge of the oxidative stress induced by tularemia. Methods. The mouse BALB/c model was chosen and the animals were infected by a dose 10 4 CFU of F. tularensis. After five days, the animals were euthanized. Blood immediately processed in plasma, spleen and liver were sampled from the cadavers. Oxidative stress markers, cytokines and histopathological were undertaken.Results. There was a significant link between oxidative stress and tularemia. Particularly elevated levels of malondialdehyde and decreased levels of low molecular weight antioxidants were found in the liver and spleen of tularemia-infected animals. The histopathological findings correlated well with the oxidative stress markers. The liver and spleen were proven to be significantly at risk from the disease and an association between stress and neutrophils in the affected organs was found. The histopathology excluded risk to other organs such as the kidney and or heart. Conclusions. Oxidative stress plays a significant role in tularemia infection in mice and this was confirmed by the histology.

show abstract

Rapid onset of ICAM-1 expression is a marker of effective macrophages activation during infection of Francisella tularensis LVS in vitro

Cited by 7 publications

References 17 publications

Arterial Hypertension Aggravates Innate Immune Responses after Experimental Stroke

Arterial Hypertension Aggravates Innate Immune Responses after Experimental Stroke

Macrophage differentiation is marked by increased abundance of the mRNA 3’ end processing machinery, altered poly(A) site usage, and sensitivity to the level of CstF64

Organs of BALB/c mice can be injured in course of tularemia

Contact Info

Product

Resources

About