Abstract
Gram-negative bacteria from the genus Acinetobacter are responsible for life-threating hospital-related infections such as pneumonia, septicemia, and meningitis, especially in immunocompromised patients. Worryingly, Acinetobacter have become multi- and extensively drug resistant (MDR/XDR) over the last few decades. The complement system is the first line of defense against microbes, thus it is highly important to increase our understanding of evasion mechanisms used by Acinetobacter spp. Here, we studied clinical isolates of Acinetobacter spp. (n=50), aiming to characterize their recognition by the complement system. Most isolates tested survived 1 h incubation in 30% serum, and only 8 isolates had a lower survival rate, yet none of those isolates were fully killed. Intriguingly, four isolates survived in human whole blood containing all cell component. Their survival was, however, significantly reduced. Flow cytometry analyses revealed that most of the isolates were detected by human IgG and IgM. Interestingly, we could not detect any significant concentration of deposited C1q, despite observing C4b deposition that was abolished in C1q-deficient serum, indicating transient binding of C1q to bacteria. Moreover, several isolates were recognized by MBL, with C4b deposition abolished in MBL-deficient serum. C3b was deposited on most isolates, but this was not, however, seen with respect to C5b and formation of the membrane attack complex (MAC), indicating that many isolates could avoid complement-mediated lysis. India ink staining showed that isolates were capsulated, and capsule thickness varied significantly between isolates. Studies performed on a wild-type strain and capsule mutant strains, demonstrated that the production of a capsular polysaccharide is one mechanism that mediates resistance to complement-mediated bactericidal activity by preventing MAC deposition and lysis. Our data showed that most clinical Acinetobacter spp. isolates are highly serum resistant despite being efficiently recognized by the complement system.
Highlights
Bacteria from the genus Acinetobacter are causing life-threating infections such as pneumonia, septicemia, and meningitis
Acinetobacter baumannii ATCC 19606 strain was purchased from the Culture Collection University of Gothenburg (CCUG) (Sweden) [36,37,38] for a total of 50 Acinetobacter strains used for the study
Being a gram-negative bacterium, Acinetobacter should theoretically be directly killed by complement once membrane attack complex (MAC) is deposited onto the bacterial surface resulting in lysis
Summary
Bacteria from the genus Acinetobacter are causing life-threating infections such as pneumonia, septicemia, and meningitis. Over the last few decades, Acinetobacter have become an increased threat to human health because of increasing multiand extensive drug resistance (MDR/XDR) among this species [1,2,3,4,5]. During the current COVID-19 pandemic, an increased number of ICU patients suffering from SARS-CoV-2 and extensive use of antibiotics has resulted in a higher number of secondary infections caused by MDR A. baumannii [11]. Besides MDR/XDR, Acinetobacter spp. are known to express several virulence factors that help them to survive in the environment, but most importantly to evade host immune system during infection [15]. The polysaccharide capsule is one of the virulence factors that protects Acinetobacter spp. from unfavorable environmental conditions as well as from phagocytosis and direct lysis by complement or killing by antimicrobial compounds [15,16,17,18]
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