What Happens When Your Body Becomes Septic

What Happens When Your Body Becomes Septic – Sepsis is one of the leading causes of death in the world and there is still no treatment other than ICU treatment. Patient outcome is determined by the complex interaction between the body’s pro- and anti-inflammatory responses, i.e. a homeostatic balance must be achieved between these two competing events for the patient to recover. However, early efforts in drug development focused primarily on controlling inflammation without any measurable results. This is despite frequent deaths during the immunoparalytic phase of the biphasic disease. Recently, attention has been paid to understanding immune paralysis (caused by apoptosis and anti-inflammatory cytokines) in order to develop therapeutic drugs. In this review, we present an argument for a good understanding of the molecular basis of inflammation and also of apoptosis in order to develop an effective therapy.

The earliest human medical records date from 1000 BC. The infection that causes sepsis is one of the biggest health problems in the world. Although the absolute global burden of this disease is difficult to determine, it is estimated that 30 million people are affected each year (Reinhart et al., 2013). The disease mainly affects low- to middle-income countries and causes approximately 6 million deaths (Fleischmann et al., 2016). Additionally, one million newborn deaths occur each year due to maternal/newborn sepsis (Vogel, 2017). In the United States alone, costs associated with this disease can exceed $16 billion, as most patients admitted to the ICU require mechanical ventilation to survive (Angus et al., 2001).

What Happens When Your Body Becomes Septic

Despite the high cost of sepsis, the cause of the disease remains mysterious. Previously, it was believed that the main source of infection came only from the gut microbiota (Friedman et al., 1998). However, later studies showed that Pseudomonas sp. Colonizing and causing upper respiratory tract infection is the most common infection in sepsis (Rangel-Frausto, 1999; Mayr et al., 2014). We now know that sepsis is a very heterogeneous disease in its cause and progression. Before the 1990s, the majority of sepsis patients presenting for examination had Gram-negative bacteria in their blood (Polat et al., 2017). This has led some scientists to establish diagnostic criteria for sepsis syndrome – statements about specific pathological symptoms and known causes of infection are central to the diagnosis (Bone et al., 1989). Over the next decade, it became apparent that although gram-negative bacteria remained prevalent in patients with sepsis, gram-positive microbiota became more prominent in patient serum (Friedman et al., 1998). . In fact, today the number of Gram-negative and Gram-positive bacteria associated with disease is about the same (Vincent and Abraham, 2006). However, the causative agent is not always bacterial because parasites and fungi can also cause sepsis (Hubner et al., 2013; Florescu and Kalil, 2014; Liang, 2016). In addition, infectious pathogens are undetectable in approximately one-third of patients (Bone et al., 1989; Liang, 2016). This includes trauma patients, who often have clinical signs of sepsis but lack bacteremia (Goris et al., 1985). These differences forced clinicians to revise the diagnostic criteria for sepsis at a consensus conference in Chicago in 1992 (Bone et al., 1992). These new criteria suggest that infection should not be limited to bacteria and that systemic inflammatory response syndrome – SIRS – has become the new age term to describe the disease (Bone et al., 1992).

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Although diagnostic criteria are updated regularly – one aspect of sepsis that has attracted the attention of researchers and remains unchanged – the presence of inflammation during the disease. The inflammatory nature of sepsis has been studied since the 1960s – where the first clinical trials were initiated to reduce the inflammatory response (Bennett et al., 1962). According to the results of these studies, corticosteroid use; However, no therapeutic benefit was noted (Bennett et al., 1962). Drug trials targeting the inflammatory phase of sepsis continued into the 2000s without providing any significant benefit to patient survival (Polat et al., 2017). A recent paradigm shift has led researchers to believe that inflammation is indeed necessary to fight disease-related infections (Ding et al., 2018). However, these discoveries are relatively new and treatments for the disease are still being researched.

Sepsis is primarily an inflammatory disease caused by the host immune response. The innate immune response is facilitated by activation of pattern recognition receptors (PRRs) during early sepsis. The receptor response is dynamic and can be induced by both pathogen-associated molecular patterns (PAMPs) and/or damage-associated molecular patterns (DAMPs) such as mitochondria released from damaged tissues (Mogensen, 2009; Hauser and Otterbein). At the organismal level, epithelial, endothelial, and complete surface receptor spreading immune surveillance cells trigger such a response (Takeuchi and Akira, 2010). Intracellular signaling processes are complex – with complementary and/or redundant roles for many signaling pathways, ultimately leading to gene expression including innate immunity and inflammation. However, uncontrolled excessive inflammation can lead to many of the symptoms seen in the early stages of sepsis, including disseminated intravascular coagulation (DIC) and subsequent dysfunction syndrome. multiorgan system (MODS), inflammation-coagulation due to abnormal activation of platelets. short Blood pressure leads to renal hypoperfusion and renal failure (Dhooria et al., 2016; Wang et al., 2018). Therefore, sepsis is a multifaceted disease that manifests in many ways, including endocrine disorders, coagulopathy, polyneuropathy, complement activation, and polyneuropathy, all of which arise from abnormal inflammation (Figure 1).

Figure 1. Sepsis is a multifaceted disease. Sepsis is characterized by multiple diseases involving various organs ranging from coagulopathy and immunosuppression to inflammation and multi-organ failure.

Inflammation is an essential step in alerting the immune system to the presence of infection so that host white blood cells can rapidly detect and fight pathogens (Weighardt et al., 2000). That response is usually tightly controlled, with inflammation gradually diminishing once the infection is over—followed by a return to baseline levels of the host’s white blood cells. When homeostasis is maintained, inflammation and excessive immune cell activity are avoided, and the immune system can mount an effective response to future infections (Newton and Dixit, 2012). During sepsis, the stimuli recognized by the immune system, from PAMPs to endotoxins and DAMPs to viruses, are much greater than during normal infections (Hotchkiss et al., 2016). The immediate result is a cytokine storm caused by overstimulation of many white blood cells that recognize these factors. Dysregulation of this response causes many of the symptoms that distinguish sepsis from normal infection, regardless of severity (Martin, 2012). When functioning normally, the immune system can fight most infections, eliminating pathogens from hosts that previously caused unbearable inflammation. The rapid resolution of most infections with little harm to the host depends on tight cytokine regulation. Cytokines are essential in initiating and enhancing innate immune responses as well as immune responses (Benner et al., 2000). However, high levels of inflammatory cytokines can be accompanied by significant innate immune suppression, which can lead to nosocomial infections (Hall et al., 2013).

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Many different antigenic agents from bacteria, viruses and fungi as well as tissue trauma are responsible for sepsis. Common pathogens isolated from patients with sepsis include gram-positive Staphylococcus aureus and Streptococcus pneumoniae and gram-negative bacteria Escherichia coli and Pseudomonas aeruginosa (Martin et al., 2003). PAMPs such as LPS are recognized by Toll-like receptors (TLRs) expressed on antigen-presenting cells (APCs), such as macrophages and dendritic cells (Poltorak et al., 1998). APCs express various TLRs containing leucine-rich repeats that sense and elicit responses against these antigens (Kawai and Akira, 2010). Once receptors interact with their recognized ligands, inflammatory mediators are recruited, some of which include mitogen-activated protein kinase (MAPK) – activated upon phosphorylation – the signal transducer and activator of transcription (STAT), Janus kinase (JAK) and nuclear. Factor κ (kappa) – light chain potentiator of activated B cells (NF-κB) – translocates to the nucleus. Consequently, gene expression is initiated to promote inflammatory cytokine and chemokine production (Johnston et al., 1995). This adaptive process relies on a series of PAMPs, DAMPs, and signaling pathways to determine the magnitude and path of the response, in an attempt to reestablish host homeostasis. During the infectious response, dysregulated internal mechanisms are associated with excessive inflammation in pathology (Surbatovic et al., 2013).

The transcriptional complex, NF-κB, is initiated in response to many extracellular inflammatory stimuli (Sen and Baltimore, 1986; Pahl, 1999). Activation of NF-κB through post-translational mechanisms induces the expression of early activator genes including IL-1/12/18 and type 1 IFN – to name a few (Naumann and Scheidereit, 1994). These inflammatory cytokines trigger the synthesis of other cytokines and chemokines, such as IL-6/8, IFN-γ and CXC chemokine ligands – promoting the inflammatory response. PRR stimulation can lead to an inflammatory response caused by immune factors

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