Neutrophil migration in infection and wound repair: going forward in reverse

Abstract

Neutrophil migration and its role during inflammation has been the focus of increased interest in the past decade. Advances in live imaging and the use of new model systems have helped to uncover the behaviour of neutrophils in injured and infected tissues. Although neutrophils were considered to be short-lived effector cells that undergo apoptosis in damaged tissues, recent evidence suggests that neutrophil behaviour is more complex and, in some settings, neutrophils might leave sites of tissue injury and migrate back into the vasculature. The role of reverse migration and its contribution to resolution of inflammation remains unclear. Here, we discuss the different cues within tissues that mediate neutrophil forward and reverse migration in response to injury or infection, and the implications of these mechanisms to human disease.

Pathogen response-like recruitment and activation of neutrophils by sterile immunogenic dying cells drives neutrophil-mediated residual cell killing

“…During pathogenic infections apart from protein PAMPs (lipoproteins/flagellin/viral proteins), cell wall-derived (LPS/lipoteichoic acid) or nucleotidic-PAMPs (viral/bacterial nucleic acids) also drive TLR signaling. 26,27 As the current setup exhibited features of pathogen responselike signaling, we wondered whether MTX-treated cells released analogous nucleotidic DAMPs. 28 Analysis of cellfree CM from MTX-treated cells revealed significant enrichment of nucleic acids (Figure 6g) including double-stranded DNA (Figure 6h).…”

“…Next, we blocked the three most important neutrophil PRRs/ receptor-adaptor systems, 12,26 that is, formyl peptide receptor 1 (FPR1), P2Rs family and MyD88 (TIR adaptor protein relevant for most TLRs, except TLR3) 7 in neutrophil-LLC cocultures (Figure 6d). Blocking P2Rs or MyD88 activity (but not FPR1) compromised neutrophil maturation (Figure 6e).…”

“…Nucleic acids-based danger signals tend to bind/signal through various cognate TLRs, for example, TLR3, TLR7/8 and TLR9. 26,27 Hence we blocked these through selective pharmacological inhibition (CU-CPT4a against TLR3) or specific oligodinucleotide (ODN) antagonists of TLR7/8 (ODN2087) or TLR9 (ODN2088). 29 Inhibition of TLR7/8/9 (wherein TLR94TLR7/8), but not TLR3, ablated neutrophil stimulation (Figure 6j).…”

Effect of Agmatine on Actin Polymerization Dynamics in Wga-Stimulated Leukocytes Under Diabetes Mellitus in Rats

“…Для того щоб проникнути крізь судинну стін-ку, лейкоцити первинно взаємодіють з ендотелієм, перекочуються по його поверхні, зазнають щільної адгезії, розпластуються і, нарешті, переміщуються крізь або між ендотеліальними клітинами кровоносної судини [11][12][13]. В адгезивних взаємодіях лейкоцитів з ендотеліоцитами безпосередню участь беруть L-, Е-і Р-селектини [14,15]. Лейкоцитарний L-селектин і глікопро-теїновий ліганд-1 для P-селектину (PSGL-1) є не лише адгезивними молекули, але і сигнальними рецептори, які зумовлюють реорганізацію цитоскелета.…”

Mkit: A cell migration assay based on microfluidic device and smartphone

“…Cell migration and chemotaxis are important for many biological and pathological processes such as host defense (de Oliveira et al 2016;Kolaczkowska and Kubes 2013), tissue development (Laird et al 2008), autoimmune disease (Luster et al 2005) and cancers (Condeelis and Segall 2003;Friedl and Wolf 2003). In-vitro real-time visualization assays are widely used for cell migration and chemotaxis research, which typically require sophisticated chemical gradient generation, controlling incubation temperature, single cell imaging and quantitative data analysis (Funamoto et al 2002;Muinonen-Martin et al 2010).…”