RESUMO
INTRODUCTION: Neutrophils are the primary effectors of the innate immune system but are profoundly histotoxic cells. The acute respiratory distress syndrome (ARDS) is considered to be a prime example of neutrophil-mediated tissue injury. SOURCES OF DATA: The information presented in this review is acquired from the published neutrophil cell biology literature and the longstanding interest of the senior authors in ARDS pathogenesis and clinical management. AREAS OF AGREEMENT: Investigators in the field would agree that neutrophils accumulate in high abundance in the pulmonary microcirculation, lung interstitium and alveolar airspace of patients with ARDS. ARDS is also associated with systemic neutrophil priming and delayed neutrophil apoptosis and clearance of neutrophils from the lungs. In animal models, reducing circulating neutrophil numbers ameliorates lung injury. AREAS OF CONTROVERSY: Areas of uncertainty include how neutrophils get stuck in the narrow pulmonary capillary network-whether this reflects changes in the mechanical properties of primed neutrophils alone or additional cell adhesion molecules, the role of neutrophil sub-sets or polarization states including pro-angiogenic and low-density neutrophils, whether neutrophil extracellular trap (NET) formation is beneficial (through bacterial capture) or harmful and the potential for neutrophils to participate in inflammatory resolution. The latter may involve the generation of specialized pro-resolving molecules (SPMs) and MMP-9, which is required for adequate matrix processing. GROWING POINTS: Different and possibly stable endotypes of ARDS are increasingly being recognized, yet the relative contribution of the neutrophil to these endotypes is uncertain. There is renewed and intense interest in understanding the complex 'new biology' of the neutrophil, specifically whether this cell might be a valid therapeutic target in ARDS and other neutrophil-driven diseases and developing understanding of ways to enhance the beneficial role of the neutrophil in the resolution phase of ARDS. AREAS TIMELY FOR DEVELOPING RESEARCH: Aside from treatment of the precipitating causes of ARDS, and scrupulous fluid, infection and ventilation management, there are no pharmacological interventions for ARDS; this represents an urgent and unmet need. Therapies aimed at reducing overall neutrophil numbers risk secondary infection; hence better ways are needed to reverse the processes of neutrophil priming activation, hyper-secretion and delayed apoptosis while enhancing the pro-resolution functions of the neutrophil.
Assuntos
Imunidade Inata/fisiologia , Neutrófilos/fisiologia , Síndrome do Desconforto Respiratório/imunologia , Lesão Pulmonar Aguda/imunologia , Endotélio/imunologia , Humanos , Infiltração de Neutrófilos/imunologia , Mucosa Respiratória/imunologiaRESUMO
This article evaluates the job quality of work in the remote gig economy. Such work consists of the remote provision of a wide variety of digital services mediated by online labour platforms. Focusing on workers in Southeast Asia and Sub-Saharan Africa, the article draws on semi-structured interviews in six countries (N = 107) and a cross-regional survey (N = 679) to detail the manner in which remote gig work is shaped by platform-based algorithmic control. Despite varying country contexts and types of work, we show that algorithmic control is central to the operation of online labour platforms. Algorithmic management techniques tend to offer workers high levels of flexibility, autonomy, task variety and complexity. However, these mechanisms of control can also result in low pay, social isolation, working unsocial and irregular hours, overwork, sleep deprivation and exhaustion.
RESUMO
BACKGROUND: In recent years, a relationship between Helicobacter pylori and many disease conditions has been reported, however, studies in its relationship with multiple sclerosis (MS) have had contradictory results. OBJECTIVE: To determine the association between the H. pylori infection and MS. METHODS: 550 patients with MS were included in the study and were matched by gender and year of birth to 299 controls. Patients were assessed for clinical and demographic parameters. An enzyme immunoassay was used to detect the presence of specific IgG antibodies against H. pylori in the serum sample of both groups. RESULTS: H. pylori seropositivity was found to be lower in the patients with MS than in controls (16% vs 21%) with the decrease pertaining to females (14% vs 22%, p=0.027) but not males (19% vs 20%, p=1.0). When adjusted for age at onset, year of birth and disease duration, H. pylori seropositive females presented with a lower disability score than seronegative females (p=0.049), while among males the reverse was true (p=0.025). There was no significant association between H. pylori seropositivity and relapse rate. CONCLUSIONS: Our results could reflect a protective role of H. pylori in the disease development. However, it may be that H. pylori infection is a surrogate marker for the 'hygiene hypothesis', a theory which postulates that early life infections are essential to prime the immune system and thus prevent allergic and autoimmune conditions later in life. The fact that the association between H. pylori seropositivity and MS risk was seen almost exclusively in females requires further investigation.