[Clinical relevance of Chlamydia pneumoniae infection--from the respiratory tract to the vascular system].
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Cardiovascular Diseases↗
Biomedical subjects
K Dalhoff
Publications and source records attributed to K Dalhoff.
Detection of Chlamydia pneumoniae within peripheral blood monocytes of patients with unstable angina or myocardial infarction.
Because individual diagnoses of vascular infection with Chlamydia pneumoniae depend entirely on surgically removed tissues, a better assay to predict vascular infection is needed. Polymerase chain reaction detection of chlamydial DNA was applied to CD14-positive cells collected from 238 patients with angiographically identified unstable angina or acute myocardial infarction. C. pneumoniae was detected in 52 (28%) of 188 persons with unstable angina and in 13 (26%) of 50 persons with myocardial infarction. Differences between groups were not significant. C. pneumoniae is present in monocytes/macrophages of a significant proportion of persons with progressive coronary artery disease. Infarction is not accompanied by a rise in chlamydial detection rates. The potential role of chlamydiae in coronary atherosclerosis may therefore be more related to acceleration of disease or systemic effects by persistent infection than to sudden initiation of infarction by acute infection.
Adult↗
Neutrophil inflammation and activation in bronchiectasis: comparison with pneumonia and idiopathic pulmonary fibrosis.
BACKGROUND: Pulmonary inflammation in bronchiectasis, pneumonia and idiopathic pulmonary fibrosis (IPF) is dominated by neutrophils. Pathophysiologic differences are seen in the degree of airway and tissue destruction. Neutrophil activation and neutrophil proteolytic activity might differ between bronchiectasis, pneumonia and IPF. OBJECTIVE: The aim of this study was to determine whether levels of inflammatory and protective markers in bronchoalveolar lavage (BAL) differed among cases of bronchiectasis, pneumonia and IPF. METHODS: We studied 11 bronchiectasis patients (group 1), 30 pneumonia patients (group 2), 15 IPF patients (group 3) and 12 healthy volunteers (group 4). In the bronchoalveolar lavage fluid, concentrations of alpha(1)-proteinase inhibitor, myeloperoxidase (MPO) and elastase-alpha(1)PI complex were determined using immunoluminometric assays. Elastase inhibition capacity (EIC) and elastase activity were determined using a colorimetric assay. RESULTS: No EIC, but free elastase activity, was found in 82% of group 1, 20% of group 2, 20% of group 3 and 0% of group 4. Median MPO concentration was highest in group 1: 7,951 ng/ml (16th-84th percentile [16-84%]: 256-36,342) vs. 692 ng/ml (106-2,279; group 2), 332 ng/ml (98-1,657; group 3), and 0.12 ng/ml (0.08-0.26; group 4). Bronchiectasis patients with bronchial Pseudomonas infection showed higher amounts of neutrophils (p < 0.01) and higher elastase activity (p < 0.05) than patients with sterile lavage. CONCLUSION: Bronchiectasis patients show a severe imbalance between neutrophil activity and protective molecules leading to possible lung destruction. Chronic Pseudomonas infection might trigger neutrophil activation. Future research and treatment strategies should focus on increased bacterial clearance and inhibition of neutrophil toxicity.
Adult↗
Decreased apoptosis and increased activation of alveolar neutrophils in bacterial pneumonia.
STUDY OBJECTIVES: The central role of apoptosis in the regulation of lung inflammation is increasingly recognized. The aim of this study was to determine the parameters of cell activation and apoptosis on neutrophils from the circulation and the pulmonary compartment in patients with community-acquired pneumonia (CAP), and to assess the role of the Fas system and of complement-regulating molecules in this context. DESIGN AND METHODS: The study population consisted of nine patients with CAP (group 1) and six age-matched control patients without evidence of bronchopulmonary inflammation (group 2). Apoptosis rate and expression of CD11b, CD16, CD55, CD59, CD95, and CD114 surface molecules on systemic and bronchoalveolar neutrophils were assessed ex vivo using fluorescence-activated cell sorter analysis. RESULTS: In patients with CAP, we found a significant decrease of the mean apoptosis rate in pulmonary neutrophils compared to systemic neutrophils, without concomitant changes in Fas expression. In contrast, cell activation markers were significantly increased on pulmonary cells (CD11b, 288 +/- 98.2 relative mean fluorescence intensity [rMFI] vs 53.8 +/- 10.8 rMFI on peripheral cells), and similar changes were observed with respect to the expression of complement-regulating molecules. Pulmonary polymorphonuclear neutrophils of the control group showed analogous changes, compared to systemic neutrophils, but a significantly higher rate of apoptosis and a lower increase of activation-marker expression were found, compared to pulmonary neutrophils of patients with pneumonia. CONCLUSIONS: Pulmonary neutrophils from patients with CAP show a decreased rate of apoptosis and increased activation status in the alveolar compartment, which may be important for effective control of pulmonary inflammation.
Adaptor Proteins, Signal Transducing↗
1,25-dihydroxycholecalciferol stimulates ICAM-1 expression of human alveolar macrophages in healthy controls and patients with sarcoidosis.
Synthesis and release of 1,25-dihydroxycholecalciferol (1, 25-(OH)2D2) by alveolar macrophages (AM) have been shown to be increased in granulomatous lung disease. ICAM-1 plays a major part in leukocyte homing to sites of chronic inflammation, which is a crucial step during the inflammatory response. Whether 1,25-(OH)2D2 alters the ICAM-1 expression of AM in humans has not been studied. Bronchoalveolar lavage (BAL) was performed in 12 healthy volunteers, in 13 patients with sarcoidosis (active disease n = 8, inactive disease n = 5), and in 9 patients with chronic bronchitis. AM were incubated with different concentrations of 1,25-(OH)2D2 (10(-11) to 10(-6) M) with and without priming with interferon-gamma (IFN-gamma) and with and without preincubation with 10(-8) M dexamethasone. In addition, the metabolites of vitamin D, 24, 25-dihydroxycholecalciferol and 25-hydroxycholecalciferol, were used. The AM expression of ICAM-1 (cELISA) and the release of tumor necrosis factor-alpha (TNF-alpha) (bioassay) by AM were determined. In healthy volunteers the ICAM-1 expression on AM was significantly and dose-dependently increased by 1,25-(OH)2D2, but not by 24, 25-dihydroxycholecalciferol and 25-hydroxycholecalciferol. Priming with IFN-gamma resulted in an additive effect. Preincubation with dexamethasone inhibited ICAM-1 expression. Addition of 1,25-(OH)2D2 after inhibition by dexamethasone increased ICAM-1 expression significantly. TNF-alpha secretion of AM from healthy volunteers was significantly reduced by 1,25-(OH)2D2. In sarcoidosis patients ICAM-1 expression was significantly higher compared with healthy volunteers. Incubation with 1,25-(OH)2D2 resulted in a further significant increase of ICAM-1 expression. TNF-alpha secretion of AM was increased compared with healthy volunteers. 1,25-(OH)2D2 reduced TNF-alpha secretion; however, this difference was not significant. 1, 25-(OH)2D2 has an immunomodulating effect on human AM both in healthy volunteers and in sarcoidosis patients with enhanced expression of ICAM-1. It may serve as an autocrine mediator in inflammatory lung disease.
Adult↗
Impaired neutrophil exocytosis in patients with severe pneumonia.
OBJECTIVE: Polymorphonuclear neutrophils (PMN) are one of the major effector cells of pulmonary defence against bacterial infection. To determine whether neutrophil function is impaired in patients with severe pneumonia, we assessed the two main partial functions exocytosis and oxidative response (ROS production) in isolated neutrophils from the peripheral venous blood of pneumonia patients and healthy volunteers. In addition, pulmonary neutrophils and peripheral neutrophils were compared in pneumonia patients. PATIENTS AND METHODS: Twenty-one patients with severe pneumonia were enrolled in the study. Eleven patients were mechanically ventilated, ten patients breathed spontaneously. For comparison, ten healthy adults were studied. The release of two markers of neutrophil exocytosis, lactoferrin and myeloperoxidase (MPO), with and without stimulation by phorbol-myristate-acetate (PMA), was determined using immunoluminometric assays. ROS production was quantified using luminol-enhanced chemiluminescence. In addition, the clinical severity of pneumonia was correlated to neutrophil exocytosis. RESULTS: With regard to blood neutrophils, both basal and PMA-stimulated exocytosis were significantly impaired in pneumonia patients compared to healthy volunteers (basal lactoferrin secretion in pneumonia patients: 0.25+/-0.36 pg/PMN versus controls: 1.17+/-0.78 pg/PMN, p<0.01). In contrast, both basal and PMA-stimulated ROS production were increased in patients compared to controls (spontaneous chemiluminescence in pneumonia patients: 13.6x10(5) cpm versus controls: 5.5x10(5) cpm). In pneumonia patients, the pulmonary neutrophils released significantly more lactoferrin, MPO and ROS compared to blood neutrophils (basal lactoferrin secretion of pulmonary neutrophils: 1.19+/-1.55 pg/PMN; p<0,01). However, after stimulation with PMA the exocytosis of pulmonary and blood neutrophils was similar. The severity of pneumonia and prognostic indices like albumin were inversely correlated to the release of lactoferrin in blood neutrophils (p<0,05). CONCLUSION: In patients with severe pneumonia, the exocytosis of blood neutrophils was significantly impaired. In contrast to this, the oxidative response was increased. Impaired bone marrow maturation of neutrophils during severe infection, perhaps due to shortened maturation time, could explain these findings.
Adult↗
[German Society of Pneumology. Recommendations for the diagnosis of nosocomial infections].
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Cross Infection↗
Endovascular presence of Chlamydia pneumoniae DNA is a generalized phenomenon in atherosclerotic vascular disease.
The common respiratory pathogen Chlamydia pneumoniae has been implicated in the pathogenesis of coronary artery disease and acute myocardial infarction. In order to verify the endovascular presence of potentially viable chlamydia by detection of genomic DNA, we examined atherosclerotic arteries from various vascular regions using a C. pneumoniae specific nested polymerase chain reaction (PCR). The samples were obtained during surgical revascularization procedures or at autopsy. Chlamydial DNA was detected in 51/238 (21%) atherosclerotic samples. A total of 17 non-atherosclerotic control samples were PCR-negative. Chlamydial presence was detected in 36/140 (26%) vascular samples obtained at coronary revascularization procedures, in 9/61 (15%) samples from carotid artery stenosis, 3/17 (18%) samples from the aorta, and 3/20 (15%) iliac artery samples. Histomorphological discrimination of infected and non-infected arterial samples was not possible. Antichlamydial IgG and IgM response as examined by microimmunofluorescence assay did not aid identification of individual endovascular infection. C. pneumoniae is present in a significant proportion of atherosclerotic arteries. Its occurrence in atheromatous plaques is not limited to coronary arteries and may be considered indicative of an infectious component in atherosclerosis. However, it remains unclear whether chlamydia actually initiates atherosclerotic injury, facilitates its progression, or merely colonizes pre-existing atheromata.
Adult↗
Early T-cell apoptosis and Fas expression during antiretroviral therapy in individuals infected with human immunodeficiency virus-1.
Several lines of evidence suggest that Fas-mediated apoptosis is involved in the CD4 T-cell depletion in human immunodeficiency virus-1 (HIV-1) infection. To investigate this, we studied changes in peripheral blood, early T-cell apoptosis and Fas expression after initiation of antiretroviral therapy (ART) in 18 HIV-1-infected individuals. Flow cytometric analysis was performed with Apostain and CD4, CD8 and Fas staining. Fas expression was quantified by standardized beads. The levels of CD4 and CD8 T cells with early apoptosis were increased comparably in HIV-1-infected individuals. Despite elevated CD4 T cell counts, no decline in early T-cell apoptosis could be detected during the first 8 weeks of ART. However, after 26 weeks of ART in five patients that showed a sustained reduction of viral replication there was a marked decrease in T cells with features of early apoptosis. No difference was found for Fas expression on early apoptotic T cells. Fas expression on CD4 and CD8 T cells was reduced after initiation of ART; this was independent of the CD4 T-cell trend and indicates that the immediate CD4 T-cell expansion during ART is probably not the result of a decreased rate of early apoptosis among peripheral blood CD4 T cells. However, preliminary data imply a long-term reduction of early T-cell apoptosis and Fas expression in patients who show a sustained reduction of viral replication.
Adult↗
Inhibition of neutrophil apoptosis and modulation of the inflammatory response by granulocyte colony-stimulating factor in healthy and ethanol-treated human volunteers.
Granulocyte colony-stimulating factor (G-CSF) has immunomodulating properties that could be beneficial for adjunctive treatment of severe infections. Cytokine release from stimulated whole blood and expression of neutrophil surface and apoptosis markers in response to G-CSF were studied in human volunteers under physiologic conditions and after ethanol pretreatment. Levels of interleukin (IL)-1 receptor antagonist and soluble tumor necrosis factor (TNF) receptor-1 were significantly increased after G-CSF, whereas TNF-alpha and IL-10 concentrations were reduced, and IL-1beta and IL-8 remained unchanged. There was a significant inhibition of neutrophil apoptosis and increased expression of complement regulatory protein CD55 without changes in CD11b, CD14, and CD59 expression. These effects were well preserved after ethanol pretreatment, which per se led to an increase in apoptosis and decreased CD55 expression. Thus, G-CSF treatment was associated with a reduction of the proinflammatory cytokine response and enhanced neutrophil survival in vivo, suggesting a therapeutic potential of G-CSF for severe infections in the nonneutropenic host.
Adult↗
Interaction of Chlamydia pneumoniae and human alveolar macrophages: infection and inflammatory response.
The obligate intracellular pathogen Chlamydia pneumoniae is associated with chronic respiratory, atherosclerotic, and rheumatic disease. The alveolar macrophage (AM) is a potential target cell for the pathogen and may contribute to respiratory immunopathology. We therefore investigated in vitro the interaction between chlamydiae and macrophages with cocultures of C. pneumoniae and AM from 12 healthy volunteers. Inflammatory responses were evaluated through lucigenin-amplified chemiluminescence; secretion of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and interleukin 8 (IL-8); and expression of intercellular adhesion molecule-1 (ICAM-1) and human leukocyte antigen-DR (HLA-DR). C. pneumoniae readily induced productive infection in the AM. Inclusions containing replicating pathogens could be maintained for up to 120 h. Morphologically similar infection patterns were seen ex vivo in AM collected from six patients with known C. pneumoniae pneumonia. AM responded to the infection with a marked, dose-dependent release of reactive oxygen species, TNF-alpha, IL-1beta, and IL-8. ICAM-1 expression remained unchanged, but HLA-DR was significantly upregulated. Our data indicate that the release of antimicrobial mediators cannot prevent chlamydial infection and replication in AM, but may be involved in amplification of the local inflammatory response in C. pneumoniae pneumonia.
Adult↗
[Recommendations for therapy of community-acquired pneumonia. German Society of Pneumology].
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Adult↗
[Incidence of bacterial pneumonia in HIV-positive patients treated with preventive co-trimoxazole or pentamidine].
BACKGROUND: Besides Pneumocystis carinii bacterial pathogens represent the most common aetiology of pulmonary infections in HIV-positive patients. However, the impact of PCP prophylaxis on the incidence of bacterial pneumonia in HIV-positive patients using pentamidine or co-trimoxazole is still unknown. PATIENTS AND METHODS: We analysed retrospectively the data of 80 consecutive HIV-positive patients with a CD4-cell count < 300/microliter. The total observation period was 1993 patient months. Type and duration of chemoprophylaxis, frequency of bacterial pneumonia, PCP, extrapulmonary bacterial infections and cerebral toxoplasmosis were documented in a standardised manner. For statistical analysis we used the Kaplan-Meier test for the time to a recurrence of the various infections under both prophylaxis regimens and the Odds ratio for determination of the relative risk. RESULTS: We followed up 47 patients inhaling 300 mg pentamidine monthly for a total of 1133 months and 33 patients taking 480 mg co-trimoxazole per day p.o. for a total of 860 months. There were no statistically significant differences between the two groups in respect of demographic parameters, stage and therapy of HIV infection and distribution of risk groups. We found seven bacterial pneumonias in the co-trimoxazole group and 13 in the pentamidine group (not significant); the most common causative organisms were S. pneumoniae (n = 4), S. aureus (n = 3) and H. influenzae (n = 3). Furthermore, in the pentamidine group 12 PCP and nine cases of toxoplasma encephalitis were observed, whereas none of these infections occurred in the co-trimoxazole group (p < 0.05). Two of the patients taking co-trimoxazole and 15 of those inhaling pentamidine had extrapulmonary bacterial infections (p < 0.05), the most frequently identified pathogen being S. aureus (n = 7). The two prophylaxis groups did not differ significantly with regard to laboratory data, course and therapy of the bacterial pneumonias. CONCLUSION: There was no significant influence of chemoprophylaxis on the incidence of bacterial pneumonia in patients with advanced HIV-disease in our study. Since S. pneumoniae represents the most common causative agent, we suggest immunisation with a polyvalent pneumococcal vaccine at an early stage of HIV-infection.
AIDS-Related Opportunistic Infections↗
[Immunosuppressive therapy in interstitial lung diseases and immunologically-induced pneumonitis].
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Arthritis, Rheumatoid↗
Production of reactive oxygen species by central venous and arterial neutrophils in severe pneumonia and cardiac lung edema.
OBJECTIVE: In pneumonia the influx of neutrophils to the lungs is thought to be of primary importance with regard to host defence and to complications like the adult respiratory distress syndrome. We wanted to evaluate the neutrophil function in patients in acute respiratory failure who required admission to the intensive care unit. DESIGN: We determined the luminolenhanced chemiluminescence (CL) of neutrophils isolated both from central venous and arterial blood. In addition, the plasma-concentrations of alpha 1-proteinase inhibitor, (alpha 1PI), alpha 2-macroglobulin (alpha 2PI) and elastase-alpha 1PI-complex (elastase) were determined by chemiluminescence immunoassay, and the intracellular elastase content of blood neutrophils was determined using immuno activation assay. PATIENTS: 28 Patients, 18 with acute pneumonia (group 1) and 10 with cardiac pulmonary edema (group 2). MEASUREMENTS AND RESULTS: In group 1, luminol enhanced CL was significantly higher than in group 2 (mean 87.7 vs 30.4 x 10(6) counts per minute, p < 0.01). The production of reactive oxygen species was significantly higher in central venous than in arterial neutrophils in the patients with pneumonia (p < 0.03). In patients with pulmonary edema there was no such difference. The plasma concentration of elastase in group 1 was significantly higher than in group 2, that of alpha 2PI were significantly lower. The intracellular elastase content of neutrophils was lower in group 1 than in group 2. In group 1, there was a trend for a correlation between lower intracellular elastase content and a higher elastase plasma concentration. There were no central venous-arterial differences with regard to leukocyte count, cell differential or protein concentration in either group. CONCLUSION: The central venous-arterial differences in neutrophil production of reactive oxygen species support the concept of compartmentalization of activated neutrophils from the systemic to the pulmonary compartment.
Adult↗
Plasma cholecystokinin and its precursors in hepatic cirrhosis.
BACKGROUND/AIMS: The liver influences the metabolism of several peptide hormones. The metabolic effect may, however, change considerably by diseases in the liver. This study examined whether hepatic cirrhosis influences the occurrence and concentrations of procholecystokinin (proCCK) and its products in plasma. METHODS: The sum of proCCK and its products (both processing intermediates and bioactive fragments) in plasma were measured by a recently developed "processing-independent analysis". Bioactive forms of CCK in plasma were measured using a highly specific radioimmunoassay directed against the C-terminal epitope of CCK. RESULTS: In plasma from patients with primary biliary cirrhosis the basal concentration of the total proCCK product was increased. Moreover, a mixed meal increased plasma concentrations of both bioactive CCK (i.e. carboxyamidated an 0-sulfated CCK peptides) and the total proCCK product in primary biliary cirrhosis. In contrast, plasma concentrations of bioactive CCK and the total proCCK product were normal in patients with alcoholic liver cirrhosis-both pre- or postprandially. The fraction of bioactive CCK in plasma from patients with both biliary and alcoholic cirrhosis was also normal. Hence, in primary biliary cirrhosis, alcoholic cirrhosis and in controls, respectively, bioactive CCK constituted 15%, 15% and 17% of the total proCCK product in the basal state; 70%, 58% and 53% 30 min after and 48%, 56% and 51% 90 min after the meal. As shown by gel chromatography, plasma from patients with primary biliary cirrhosis and controls sampled 30 min after a meal contained CCK-33, -22 and -8-like peptides. In addition, plasma contained non-amidated (approximately non-bioactive) proCCK products corresponding in size to CCK-83, -58 and -33. Ninety minutes after a meal, CCK-8 predominated in plasma from patients with primary biliary cirrhosis, whereas plasma from controls displayed a CCK profile similar to that obtained 30 min post-prandially. CONCLUSIONS: The results show that CCK-8 is metabolized at a slower rate in patients with primary biliary cirrhosis.
Adult↗
Expression of liver functions following sub-lethal and non-lethal doses of allyl alcohol and acetaminophen in the rat.
BACKGROUND/AIMS: To relate severity of intoxication with allyl alcohol and acetaminophen to modulated hepatic gene expression of liver functions and regeneration. METHODS: Rats fasted for 12 h received acetaminophen 3.5 or 5.6 g per kg body weight, or allyl alcohol 100 or 125 microl by gastric tube, doses producing no and about 30% mortality, respectively, within 2 days. In the morning 2, 6, 12, 24, and 36 h after intoxication, RNA was extracted from liver tissue. By slot blot hybridization mRNA levels were determined for acute phase proteins, enzymes involved in ammonia elimination and urea synthesis, and for proteins related to liver regeneration. RESULTS: After allyl alcohol, mRNA of "positive" acute phase proteins was higher than after acetaminophen and increased with the dose, whereas after acetaminophen it decreased with the dose. The mRNA of the urea cycle enzymes and glutamine synthetase was uniformly reduced by allyl alcohol, whereas that of most urea cycle enzymes was above the controls after the non-lethal, but not after the sub-lethal, dose of acetaminophen. The mRNA of glutamine synthetase was significantly more reduced by acetaminophen than by allyl alcohol. The mRNA of cell-cycle dependent proteins was greatly reduced after both toxins, more after the higher dose. CONCLUSIONS: The study shows that acetaminophen intoxication inhibits or fails to induce the expression of acute phase proteins in contrast to allyl alcohol intoxication. Allyl alcohol suppressed the expression of urea cycle enzymes, whereas that of the rate limiting enzymes carbamoylphosphate synthase and argininosuccinate synthetase was increased by the non-lethal but not by the sub-lethal dose of acetaminophen. The expression of the cell-cycle dependent proteins was more suppressed after the sub-lethal than after the non-lethal dose of both toxins. The data support the view that a fatal outcome of the intoxications depends more on the ability to regenerate than on the maintenance of liver-specific functions.
1-Propanol↗
Different BALF protein composition in normal children and adults.
UNLABELLED: Quantification of proteins in bronchoalveolar lavage fluid (BALF) is being performed increasingly, because of their potency in elucidating pathophysiological processes and their possible clinical relevance. STUDY POPULATION: 37 normal children (12 female, 25 male, mean age +/- SD 7.9 +/- 3.5 years, range 3-16 years) undergoing elective surgery for nonpulmonary illnesses and 16 healthy adults (all male, mean age +/- SD 24.7 +/- 2.6 years, range 20-28 years, 8 smokers, 8 nonsmokers) have been studied after approval by the ethics committees of both institutions. METHODS: BAL was performed with normal saline in the right middle lobe or one of its segments. Lavage volume was 15 x 20 ml in adults and 3 x 1 ml/kg in children. In adults the first aliquot was processed separately, 2 aliquots of the following were pooled (resulting in 8 different fractions) so that different lavage protocols could be calculated. The concentrations of the plasma-proteins alpha 1-proteinase inhibitor (alpha-1PI), alpha 2-macroglobulin (alpha 2PI), albumin (Alb) and of the locally released proteins myeloperoxidase (MPO), lactoferrin (Lf), elastase (Ela) and fibronectin (Fib) were determined in BALF using chemiluminescence immunoassays. RESULTS: The BALF concentrations of the plasma proteins were higher in children compared to adults. In contrast, concentrations of the locally released proteins were similar in both groups. Protein concentrations in the first recovered aliquot were different from the following in healthy adults with higher values of MPO, Lf and Ela and lower concentrations of alpha 1PI, alpha 2PI and Alb. Subsequent aliquots did not show a progressive dilution of these proteins with increasing lavage volumes. In smokers, BALF concentrations of albumin, alpha 1PI and MPO were higher compared to nonsmokers. CONCLUSION: BALF protein concentrations are different in normal children and adults. These results underscore the necessity to establish independent reference values for children, as could be demonstrated earlier with regard to BAL cell composition.
Adult↗